Neuroprotective Effects of Sodium Butyrate by Restoring Gut Microbiota and Inhibiting TLR4 Signaling in Mice with MPTP-Induced Parkinson’s Disease
Open accessAbstract
Parkinson’s disease (PD) is a prevalent type of neurodegenerative disease. There is mounting evidence that the gut microbiota is involved in the pathogenesis of PD. Sodium butyrate (NaB) can regulate gut microbiota and improve brain functioning in neurological disorders. Hence, we examined whether the neuroprotective function of NaB on PD was mediated by the modulation of gut microbial dysbiosis and revealed its possible mechanisms. Mice were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days to construct the PD model. NaB gavage was given 2 h after the daily MPTP injections for 21 days. NaB improved the motor functioning of PD mice, increased striatal neurotransmitter levels, and reduced the death of dopaminergic neurons. The 16S rRNA sequencing analysis revealed that NaB restored the gut microbial dysbiosis. NaB also attenuated the intestinal barrier’s disruption and reduced serum, colon, and striatal pro-inflammatory cytokines, along with inhibiting the overactivation of glial cells, suggesting an inhibitory effect on inflammation from NaB throughout the gut–brain axis of the PD mice. Mechanistic studies revealed that NaB treatment suppressed the TLR4/MyD88/NF-kB pathway in the colon and striatum. In summary, NaB had a neuroprotective impact on the PD mice, likely linked to its regulation of gut microbiota to inhibit gut–brain axis inflammation.
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TL;DR
Sodium butyrate (NaB) improved motor function, restored striatal neurotransmitters and dopaminergic neurons, and reduced gut–brain-axis inflammation in MPTP-induced Parkinson’s disease (PD) mice. Its neuroprotective effects were associated with remodeling gut microbiota, repairing the intestinal barrier, and inhibiting TLR4/MyD88/NF-κB signaling in the colon and striatum.
Key findings
- NaB improved motor behavior: MPTP mice had longer pole-test time and shorter rotarod time (p < 0.001), while MPTP + NaB mice performed significantly better on both (p < 0.001); open-field total distance, central distance, and central crossings were also improved (p < 0.001).
- NaB increased striatal DA by 49.2% and 5-HT by 49.2% versus MPTP (p < 0.01 for both), after MPTP reduced DA by 31.5% and 5-HT by 34.6%; DOPAC and 5-HIAA rose 38.7% and 32.0% with NaB (p < 0.05). TH+ neurons fell 51.2% in PD mice, and NaB inhibited this decline by 83.0%; striatal TH protein fell 47.5% and NaB increased it by 93.0%.
- NaB attenuated glial activation: striatal Iba-1 was 102.2% higher in MPTP mice and decreased 45.4% with NaB (p < 0.001); GFAP was reported 53.6% lower in MPTP mice and decreased 26.2% with NaB (p < 0.01).
- NaB restored gut microbiota and barrier/inflammation markers: MPTP increased Verrucomicrobiota and Proteobacteria, Bacteroidaceae, Bacteroides, Parabacteroides, Akkermansia, and Lactobacillus, and reduced Erysipelotrichaceae, Dubosiella, and Odoribacter; NaB shifted these changes. Colonic ZO-1 and occludin fell 32.1% and 55.8% in MPTP mice and increased 49.2% and 100.5% with NaB; serum IL-6 and TNF-α rose 193.6% and 150.5% and fell 64.2% and 50.0% with NaB; striatal TLR4/MyD88/NF-κB rose 78.4%, 75.8%, and 91.6% and fell 45.4%, 44.1%, and 45.9% with NaB.
Methods
- Male C57BL/6 mice, 7 weeks old, were randomized into control, MPTP, and MPTP + NaB groups (n = 12 per group). PD was induced with 30 mg/kg MPTP intraperitoneally for 7 consecutive days; NaB or saline was given intragastrically 2 h after daily MPTP injections for 21 days.
- Behavioral tests included pole, rotarod, and open-field tests. Striatal neurotransmitters were measured by HPLC; TH, glial, barrier, and TLR4/MyD88/NF-κB proteins by immunofluorescence and Western blot; gut microbiota by 16S rRNA V3–V4 sequencing; colon pathology by H&E; serum cytokines by ELISA.
- Statistical analysis used one-way ANOVA with Tukey’s post-hoc test, and Kruskal–Wallis with Dunn’s or Wilcoxon tests for microbiota comparisons; p < 0.05 was significant. Feces and fresh tissues were collected from 7 mice per group, and 5 mice per group were used for staining.
Limitations
- Stated: the study was limited to animals, and applicability to clinical populations remains a major challenge; further investigation is needed to demonstrate NaB regulation of gut microbiota structure. The authors also note that NaB’s effect on α-diversity was statistically insignificant and suggest increasing sample size.
- Evident: causality is not established because there was no germ-free, fecal microbiota transplantation, or TLR4 knockout experiment; only male mice were used; no dose–response analysis is reported; and several microbiota changes after NaB are reported as p > 0.05 despite directional shifts.
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- Findingown data
NaB treatment decreased Iba-1 expression in the striatum by 45.4% compared to MPTP-treated mice (p < 0.001).
“while the NaB treatment in the mice with MPTP-induced PD decreased its expression by 45.4% compared to the MPTP-treated mice (p < 0.001) (Figure 4A).”
Quote in the paperSubstantial claim - Findingown data
MPTP-induced mice exhibited a considerably longer pole test time than control mice (p < 0.001).
“In comparison to the control mice, the MPTP-induced mice exhibited severe locomotor impairment, as shown by a considerably longer pole test time and a considerably shorter rotarod test time (p < 0.001).”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice exhibited significantly better performance in the pole test than MPTP mice (p < 0.001).
“In contrast, the MPTP + NaB mice exhibited significantly better performance in the pole test (p < 0.001) and rotarod test (p < 0.001) relative to the MPTP mice (Figure 1B,C).”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a 32.0% increase in striatal 5-HIAA levels compared to MPTP mice (p < 0.05).
“The striatal levels of DOPAC and 5-HIAA were elevated remarkably in the MPTP + NaB group by 38.7% and 32.0%, respectively, compared to the MPTP group (p < 0.05 for both) (Figure 2C,D).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had a smaller central distance in the open field test than control mice (p < 0.001).
“A lesser total distance (p < 0.001), a smaller central distance (p < 0.001), and fewer crossings in the central zone (p < 0.001) were found in MPTP mice relative to the control mice.”
Quote in the paperSubstantial claim
- Findingown data
MPTP-induced mice exhibited a considerably shorter rotarod test time than control mice (p < 0.001).
“In comparison to the control mice, the MPTP-induced mice exhibited severe locomotor impairment, as shown by a considerably longer pole test time and a considerably shorter rotarod test time (p < 0.001).”
Quote in the paperSubstantial claim - Findingown data
NaB exposure inhibited the decline in TH+ dopaminergic neurons by 83.0% compared to the MPTP group (p < 0.05).
“but NaB exposure inhibited the decline by 83.0% compared to the MPTP group (p < 0.05) (Figure 3A,B).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had a 34.6% decrease in striatal 5-HT levels compared to control mice (p < 0.01).
“Additionally, 5-HT levels decreased by 34.6% in the MPTP mice (p < 0.01)”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a greater total distance in the open field test than MPTP mice (p < 0.001).
“The performance in terms of the total distance (p < 0.001), central distance (p < 0.001), and the total number of crossings in the central zone (Figure 1E–G) (p < 0.001) was better for the MPTP + NaB mice relative to the MPTP mice.”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had more crossings in the central zone in the open field test than MPTP mice (p < 0.001).
“The performance in terms of the total distance (p < 0.001), central distance (p < 0.001), and the total number of crossings in the central zone (Figure 1E–G) (p < 0.001) was better for the MPTP + NaB mice relative to the MPTP mice.”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had a 31.5% decrease in striatal DA levels compared to control mice (p < 0.01).
“A 31.5% decrease in DA levels in the striatum of MPTP mice (p < 0.01) was observed.”
Quote in the paperSubstantial claim - Findingown data
Iba-1 levels in the striatum of PD mice were 102.2% higher than in control mice (p < 0.001).
“in the striatum of the PD mice, Iba-1 levels were substantially higher by 102.2% (p < 0.001)”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had a lesser total distance in the open field test than control mice (p < 0.001).
“A lesser total distance (p < 0.001), a smaller central distance (p < 0.001), and fewer crossings in the central zone (p < 0.001) were found in MPTP mice relative to the control mice.”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a 38.7% increase in striatal DOPAC levels compared to MPTP mice (p < 0.05).
“The striatal levels of DOPAC and 5-HIAA were elevated remarkably in the MPTP + NaB group by 38.7% and 32.0%, respectively, compared to the MPTP group (p < 0.05 for both) (Figure 2C,D).”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a greater central distance in the open field test than MPTP mice (p < 0.001).
“The performance in terms of the total distance (p < 0.001), central distance (p < 0.001), and the total number of crossings in the central zone (Figure 1E–G) (p < 0.001) was better for the MPTP + NaB mice relative to the MPTP mice.”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a 49.2% increase in striatal DA levels compared to MPTP mice (p < 0.01).
“In contrast, DA levels in the striatum increased remarkably by 49.2% in the MPTP + NaB mice (p < 0.01) relative to the MPTP mice (Figure 2A).”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice exhibited significantly better performance in the rotarod test than MPTP mice (p < 0.001).
“In contrast, the MPTP + NaB mice exhibited significantly better performance in the pole test (p < 0.001) and rotarod test (p < 0.001) relative to the MPTP mice (Figure 1B,C).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had fewer crossings in the central zone in the open field test than control mice (p < 0.001).
“A lesser total distance (p < 0.001), a smaller central distance (p < 0.001), and fewer crossings in the central zone (p < 0.001) were found in MPTP mice relative to the control mice.”
Quote in the paperSubstantial claim - Findingown data
MPTP + NaB mice had a 49.2% increase in striatal 5-HT levels compared to MPTP mice (p < 0.01).
“whereas these increased by 49.2% in the MPTP + NaB mice (p < 0.01) (Figure 2B).”
Quote in the paperSubstantial claim - Findingown data
NaB treatment increased striatal TH expression by 93.0% compared to MPTP alone (p < 0.01).
“while the NaB treatment increased the TH expression significantly (p < 0.01) by 93.0% compared to MPTP alone (Figure 3C,D).”
Quote in the paperSubstantial claim - Findingown data
Western blotting showed that TH levels in the striatum of MPTP mice decreased by 47.5% compared to control mice (p < 0.01).
“Consistently, the Western blotting demonstrated that the TH levels in the MPTP mice decreased remarkably by 47.5% (p < 0.01) compared to the control mice”
Quote in the paperSubstantial claim - Findingown data
Colonic IL-6 levels increased by 83.6% in MPTP mice compared to control (p < 0.05).
“The colonic TNF-α and IL-6 levels increased remarkably by 88.2% and 83.6% in the MPTP mice (p < 0.001, p < 0.05, respectively)”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment reversed the loss of TH-positive cells in the substantia nigra of Parkinson's disease mice.
“The NaB treatment reversed the loss of TH-positive cells in the substantia nigra of the PD mice, as well as the decline in DA and TH levels in the striatum, consistent with previous findings [23,25].”
Quote in the paperSubstantial claim - Findingown data
ZO-1 expression was reduced by 32.1% in the colon of MPTP mice compared to control (p < 0.05).
“The expression levels of ZO-1 and occludin were reduced remarkably by 32.1% and 55.8%, respectively, in the colon of the MPTP mice (p < 0.05 and p < 0.01, respectively)”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had higher relative abundance of Lactobacillus (p < 0.05).
“In terms of the bacterial genera, the MPTP mice had higher relative abundances of Bacteroides, Parabacteroides, Akkermansia, and Lactobacillus (p < 0.01, p < 0.01, p < 0.01, p < 0.05, respectively)”
Quote in the paperNot a substantial claim - Findingown data
Sodium butyrate treatment inhibited neuroinflammation in MPTP-induced Parkinson's disease mice.
“According to the results of this study, NaB improved gut microbial dysbiosis and inhibited intestinal inflammation and neuroinflammation, resulting in neuroprotective effects, which involved the TLR4/MyD88/NF-κB pathway.”
Quote in the paperSubstantial claim - Findingown data
Colonic NF-κB protein expression decreased by 94.2% in the PD group mice compared to control (p < 0.05).
“Similarly, TLR4, MyD88, and NF-B protein expression decreased nearly 70%, 94.7%, and 94.2% in the colons of the PD group mice, respectively (p < 0.01, p < 0.05, p < 0.05, respectively).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had higher relative abundance of Parabacteroides (p < 0.01).
“In terms of the bacterial genera, the MPTP mice had higher relative abundances of Bacteroides, Parabacteroides, Akkermansia, and Lactobacillus (p < 0.01, p < 0.01, p < 0.01, p < 0.05, respectively)”
Quote in the paperNot a substantial claim - Findingown data
Proteobacteria abundance was elevated in the PD mice (p < 0.05).
“In terms of the phylum level, Verrucomicrobiota and Proteobacteria were elevated in the PD mice (p < 0.001, p < 0.05, respectively)”
Quote in the paperSubstantial claim - Findingown data
NaB administration decreased relative abundance of Parabacteroides (p > 0.05).
“However, the relative abundance of Parabacteroides, Bacteroides, Akkermansia, and Lactobacillus decreased after NaB administration (p > 0.05, p < 0.05, p > 0.05, p < 0.05, correspondingly)”
Quote in the paperNot a substantial claim - Findingown data
Colonic TNF-α levels decreased by 45.0% in MPTP + NaB mice compared to MPTP mice (p < 0.001).
“whereas these levels correspondingly decreased by 45.0% and 42.0% in the MPTP + NaB mice (p < 0.001, p < 0.05, respectively) (Figure 7F–H).”
Quote in the paperSubstantial claim - Findingown data
MPTP treatment increased the gut microbiota's alpha-diversity in mice.
“The MPTP treatment increased the gut microbiota’s α-diversity.”
Quote in the paperNot a substantial claim - Findingown data
NaB group had elevated abundance of Erysipelotrichaceae (p > 0.05).
“whereas that of Erysipelotrichaceae was elevated considerably (p > 0.05).”
Quote in the paperNot a substantial claim - Findingown data
NaB restored the gut microbial dysbiosis in PD mice.
“The 16S rRNA sequencing analysis revealed that NaB restored the gut microbial dysbiosis.”
Quote in the paperSubstantial claim - Findingown data
MPTP mice recorded an increased abundance of Bacteroidaceae (p < 0.001).
“In terms of the family level, the MPTP mice recorded an increased abundance of Bacteroidaceae (p < 0.001)”
Quote in the paperNot a substantial claim - Findingown data
MPTP mice had lowered relative abundance of Odoribacter (p < 0.01).
“while those of Dubosiella and Odoribacter in the MPTP group were lowered (p < 0.05, p < 0.01, respectively).”
Quote in the paperNot a substantial claim - Findingown data
NaB-treated mice showed significantly lower HE histological scores (p < 0.05).
“whereas the NaB-treated mice showed significantly lower scores (p < 0.05) (Figure 6B).”
Quote in the paperSubstantial claim - Findingown data
There was a significant difference in the gut microbiota overall structure across the control, MPTP, and MPTP + NaB mice.
“A significant difference in the gut microbiota was observed, indicating substantial variations in the overall structure of the gut microbiota across the control, MPTP, and MPTP + NaB mice.”
Quote in the paperSubstantial claim - Findingown data
NaB administration elevated relative abundance of Dubosiella (p > 0.05).
“whereas that of Dubosiella and Odoribacter was elevated substantially (p > 0.05, p < 0.05, respectively) (Figure 5G).”
Quote in the paperNot a substantial claim - Findingown data
NaB treatment decreased GFAP expression in the striatum by 26.2% in MPTP mice (p < 0.01).
“The treatment with NaB decreased GFAP expression (p < 0.01) by 26.2% in the MPTP mice (Figure 4B,C).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice recorded a reduction in Erysipelotrichaceae abundance (p < 0.05).
“along with a reduction in Erysipelotrichaceae abundance (p < 0.05).”
Quote in the paperNot a substantial claim - Findingown data
NaB reduced serum, colon, and striatal pro-inflammatory cytokines in PD mice.
“reduced serum, colon, and striatal pro-inflammatory cytokines”
Quote in the paperSubstantial claim - Findingown data
In MPTP + NaB mice, striatal NF-κB levels declined by 45.9% compared to MPTP mice (p < 0.01).
“whereas these levels declined significantly by 45.4%, 44.1%, and 45.9% in the MPTP + NaB mice (p < 0.05, p < 0.001, p < 0.01, respectively) (Figure 7I–L).”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment inhibited the abnormal increase in the abundance of Proteobacteria in Parkinson's disease mice.
“Notably, the NaB treatment inhibited the abnormal increase in the abundances of Proteobacteria, Bacteroides, and Akkermansia, which might exert beneficial effects on the PD mice.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment inhibited intestinal inflammation in MPTP-induced Parkinson's disease mice.
“According to the results of this study, NaB improved gut microbial dysbiosis and inhibited intestinal inflammation and neuroinflammation, resulting in neuroprotective effects, which involved the TLR4/MyD88/NF-κB pathway.”
- Also stated in: § 4. Discussion · plain
“All of these results indicated an intense intestinal inflammatory response in the PD mice, and the NaB treatment significantly reduced intestinal inflammation.”
Quote in the paperSubstantial claim - Also stated in: § 4. Discussion · plain
- Findingown data
In MPTP + NaB mice, striatal TLR4 levels declined by 45.4% compared to MPTP mice (p < 0.05).
“whereas these levels declined significantly by 45.4%, 44.1%, and 45.9% in the MPTP + NaB mice (p < 0.05, p < 0.001, p < 0.01, respectively) (Figure 7I–L).”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment inhibited the abnormal increase in the abundance of Bacteroides in Parkinson's disease mice.
“Notably, the NaB treatment inhibited the abnormal increase in the abundances of Proteobacteria, Bacteroides, and Akkermansia, which might exert beneficial effects on the PD mice.”
Quote in the paperSubstantial claim - Findingown data
Serum TNF-α levels were higher by 150.5% in MPTP mice compared to control (p < 0.001).
“The ELISA findings illustrated that the IL-6 and TNF-α levels in the serum were higher by 193.6% and 150.5%, respectively, in MPTP mice (p < 0.001 for both)”
Quote in the paperSubstantial claim - Findingown data
Serum IL-6 levels decreased by 64.2% in MPTP + NaB mice compared to MPTP mice (p < 0.001).
“whereas these levels decreased correspondingly by 64.2% and 50.0% in the MPTP + NaB mice (p < 0.001 for both) (Figure 7A,B).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had higher relative abundance of Akkermansia (p < 0.01).
“In terms of the bacterial genera, the MPTP mice had higher relative abundances of Bacteroides, Parabacteroides, Akkermansia, and Lactobacillus (p < 0.01, p < 0.01, p < 0.01, p < 0.05, respectively)”
Quote in the paperNot a substantial claim - Findingown data
Colonic MyD88 protein expression decreased by 94.7% in the PD group mice compared to control (p < 0.05).
“Similarly, TLR4, MyD88, and NF-B protein expression decreased nearly 70%, 94.7%, and 94.2% in the colons of the PD group mice, respectively (p < 0.01, p < 0.05, p < 0.05, respectively).”
Quote in the paperSubstantial claim - Findingown data
Striatal TLR4 levels increased by 78.4% in PD mice compared to control (p < 0.05).
“the TLR4, MyD88, and NF-κB levels increased significantly in the striatum by 78.4%, 75.8%, and 91.6%, respectively, in the PD mice (p < 0.05, p < 0.001, p < 0.01, respectively)”
Quote in the paperSubstantial claim - Findingown data
The abundance of Akkermansia was significantly elevated in mice with Parkinson's disease.
“The abundance of Akkermansia was found to be significantly elevated in mice with PD consistently in our study.”
Quote in the paperSubstantial claim - Findingown data
MPTP mice showed significantly higher HE histological scores (p < 0.01).
“Moreover, the MPTP mice showed significantly higher HE histological scores (p < 0.01)”
Quote in the paperSubstantial claim - Findingown data
The MPTP group exhibited significantly higher Simpson index than controls.
“The MPTP group exhibited significantly higher Shannon and Simpson indexes relative to the controls.”
Quote in the paperNot a substantial claim - Findingown data
NaB administration elevated relative abundance of Odoribacter (p < 0.05).
“whereas that of Dubosiella and Odoribacter was elevated substantially (p > 0.05, p < 0.05, respectively) (Figure 5G).”
Quote in the paperNot a substantial claim - Findingcitation
Sodium butyrate treatment reversed the decline in DA and TH levels in the striatum of Parkinson's disease mice.
“The NaB treatment reversed the loss of TH-positive cells in the substantia nigra of the PD mice, as well as the decline in DA and TH levels in the striatum, consistent with previous findings [23,25].”
Quote in the paperSubstantial claim - Findingown data
NaB exposure decreased colonic NF-κB protein expression by 48.0% compared to MPTP mice (p < 0.05).
“In contrast, NaB exposure substantially decreased these protein expression levels by 41.2%, 67.0%, and 48.0% (p < 0.01, p < 0.01, p < 0.05, respectively) (Figure 7M–P).”
Quote in the paperSubstantial claim - Findingown data
The 16S rRNA data showed abnormal microbial compositions at different taxonomic levels in Parkinson's disease mice.
“Furthermore, the 16S rRNA data showed abnormal microbial compositions at different taxonomic levels.”
Quote in the paperSubstantial claim - Findingown data
Striatal TNF-α levels declined by 78.7% in MPTP mice compared to control (p < 0.01).
“The Western blotting illustrated a substantial decline in the levels of TNF-α and IL-6 of 78.7% and 55.1%, respectively, in the striatum of the MPTP mice (p < 0.01, p < 0.05)”
Quote in the paperSubstantial claim - Findingown data
Colonic TNF-α levels increased by 88.2% in MPTP mice compared to control (p < 0.001).
“The colonic TNF-α and IL-6 levels increased remarkably by 88.2% and 83.6% in the MPTP mice (p < 0.001, p < 0.05, respectively)”
Quote in the paperSubstantial claim - Findingown data
Colonic TLR4 protein expression decreased nearly 70% in the PD group mice compared to control (p < 0.01).
“Similarly, TLR4, MyD88, and NF-B protein expression decreased nearly 70%, 94.7%, and 94.2% in the colons of the PD group mice, respectively (p < 0.01, p < 0.05, p < 0.05, respectively).”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had lowered relative abundance of Dubosiella (p < 0.05).
“while those of Dubosiella and Odoribacter in the MPTP group were lowered (p < 0.05, p < 0.01, respectively).”
Quote in the paperNot a substantial claim - Findingown data
Serum TNF-α levels decreased by 50.0% in MPTP + NaB mice compared to MPTP mice (p < 0.001).
“whereas these levels decreased correspondingly by 64.2% and 50.0% in the MPTP + NaB mice (p < 0.001 for both) (Figure 7A,B).”
Quote in the paperSubstantial claim - Findingown data
Serum IL-6 levels were higher by 193.6% in MPTP mice compared to control (p < 0.001).
“The ELISA findings illustrated that the IL-6 and TNF-α levels in the serum were higher by 193.6% and 150.5%, respectively, in MPTP mice (p < 0.001 for both)”
Quote in the paperSubstantial claim - Findingown data
The NaB group exhibited lower colonic inflammation than the MPTP group.
“The NaB group exhibited lower colonic inflammation than the MPTP group (Figure 6A).”
Quote in the paperSubstantial claim - Findingown data
NaB group had lowered abundance of Bacteroidaceae (p < 0.05).
“However, the abundance of Bacteroidaceae was lowered in the NaB group (p < 0.05)”
Quote in the paperNot a substantial claim - Findingown data
Colonic IL-6 levels decreased by 42.0% in MPTP + NaB mice compared to MPTP mice (p < 0.05).
“whereas these levels correspondingly decreased by 45.0% and 42.0% in the MPTP + NaB mice (p < 0.001, p < 0.05, respectively) (Figure 7F–H).”
Quote in the paperSubstantial claim - Findingown data
NaB administration decreased relative abundance of Bacteroides (p < 0.05).
“However, the relative abundance of Parabacteroides, Bacteroides, Akkermansia, and Lactobacillus decreased after NaB administration (p > 0.05, p < 0.05, p > 0.05, p < 0.05, correspondingly)”
Quote in the paperSubstantial claim - Findingown data
NaB administration decreased relative abundance of Akkermansia (p > 0.05).
“However, the relative abundance of Parabacteroides, Bacteroides, Akkermansia, and Lactobacillus decreased after NaB administration (p > 0.05, p < 0.05, p > 0.05, p < 0.05, correspondingly)”
Quote in the paperNot a substantial claim - Findingown data
The abundance of Bacteroides increased significantly in Parkinson's disease mice.
“The abundance of Bacteroides also increased significantly in PD mice and is known to correlate with an increase in plasma TNF-α and interferon-γ levels in patients with PD [49].”
Quote in the paperNot a substantial claim - Findingown data
Striatal MyD88 levels increased by 75.8% in PD mice compared to control (p < 0.001).
“the TLR4, MyD88, and NF-κB levels increased significantly in the striatum by 78.4%, 75.8%, and 91.6%, respectively, in the PD mice (p < 0.05, p < 0.001, p < 0.01, respectively)”
Quote in the paperSubstantial claim - Findingown data
NaB treatment lowered striatal IL-6 expression by 37.9% compared to MPTP mice (p < 0.05).
“while the NaB treatment considerably lowered the corresponding expression levels by 41.0% and 37.9% (p < 0.01, p < 0.05, respectively) (Figure 7C–E).”
Quote in the paperSubstantial claim - Findingown data
NaB exposure decreased colonic MyD88 protein expression by 67.0% compared to MPTP mice (p < 0.01).
“In contrast, NaB exposure substantially decreased these protein expression levels by 41.2%, 67.0%, and 48.0% (p < 0.01, p < 0.01, p < 0.05, respectively) (Figure 7M–P).”
Quote in the paperSubstantial claim - Findingown data
NaB exposure decreased colonic TLR4 protein expression by 41.2% compared to MPTP mice (p < 0.01).
“In contrast, NaB exposure substantially decreased these protein expression levels by 41.2%, 67.0%, and 48.0% (p < 0.01, p < 0.01, p < 0.05, respectively) (Figure 7M–P).”
Quote in the paperSubstantial claim - Findingown data
NaB reduced the death of dopaminergic neurons in PD mice.
“NaB improved the motor functioning of PD mice, increased striatal neurotransmitter levels, and reduced the death of dopaminergic neurons.”
Quote in the paperSubstantial claim - Findingown data
The abundance of Proteobacteria was remarkably elevated in Parkinson's disease mice.
“A remarkable elevation in the abundance of Proteobacteria was noted in the PD mice, consistent with previous reports on PD patients’ gut microbiota [46,47].”
Quote in the paperSubstantial claim - Findingown data
MPTP mice had higher relative abundance of Bacteroides (p < 0.01).
“In terms of the bacterial genera, the MPTP mice had higher relative abundances of Bacteroides, Parabacteroides, Akkermansia, and Lactobacillus (p < 0.01, p < 0.01, p < 0.01, p < 0.05, respectively)”
Quote in the paperNot a substantial claim - Findingown data
Striatal IL-6 levels declined by 55.1% in MPTP mice compared to control (p < 0.05).
“The Western blotting illustrated a substantial decline in the levels of TNF-α and IL-6 of 78.7% and 55.1%, respectively, in the striatum of the MPTP mice (p < 0.01, p < 0.05)”
Quote in the paperSubstantial claim - Findingown data
The MPTP group exhibited significantly higher Shannon index than controls.
“The MPTP group exhibited significantly higher Shannon and Simpson indexes relative to the controls.”
Quote in the paperNot a substantial claim - Findingown data
Occludin expression was reduced by 55.8% in the colon of MPTP mice compared to control (p < 0.01).
“The expression levels of ZO-1 and occludin were reduced remarkably by 32.1% and 55.8%, respectively, in the colon of the MPTP mice (p < 0.05 and p < 0.01, respectively)”
Quote in the paperSubstantial claim - Findingown data
In MPTP + NaB mice, occludin levels increased by 100.5% compared to MPTP mice (p < 0.01).
“whereas in the MPTP + NaB mice, the occludin and ZO-1 levels increased by 100.5% and 49.2% (p < 0.01 and p < 0.05, respectively) (Figure 6D,E).”
Quote in the paperSubstantial claim - Findingown data
NaB inhibited the overactivation of glial cells in PD mice.
“along with inhibiting the overactivation of glial cells”
Quote in the paperSubstantial claim - Findingown data
Striatal NF-κB levels increased by 91.6% in PD mice compared to control (p < 0.01).
“the TLR4, MyD88, and NF-κB levels increased significantly in the striatum by 78.4%, 75.8%, and 91.6%, respectively, in the PD mice (p < 0.05, p < 0.001, p < 0.01, respectively)”
Quote in the paperSubstantial claim - Findingown data
NaB attenuated the intestinal barrier's disruption in PD mice.
“NaB also attenuated the intestinal barrier’s disruption”
Quote in the paperSubstantial claim - Findingown data
NaB administration decreased relative abundance of Lactobacillus (p < 0.05).
“However, the relative abundance of Parabacteroides, Bacteroides, Akkermansia, and Lactobacillus decreased after NaB administration (p > 0.05, p < 0.05, p > 0.05, p < 0.05, correspondingly)”
Quote in the paperNot a substantial claim - Findingown data
GFAP expression in the striatum of MPTP mice decreased by 53.6% compared to control mice (p < 0.001).
“As well, the MPTP mice displayed a 53.6% decrease in GFAP expression compared to the control mice in the striatum (p < 0.001).”
Quote in the paperNot a substantial claim - Findingown data
The MPTP group showed more severe colonic inflammation relative to the control group.
“The MPTP group showed more severe colonic inflammation relative to the control group.”
Quote in the paperSubstantial claim - Findingown data
The microbial community morphologies of the sodium butyrate-treated and control groups were similar in beta-diversity analysis.
“The β-diversity analysis demonstrated that the microbial community morphologies of the NaB-treated and control groups were similar.”
Quote in the paperNot a substantial claim - Findingown data
In MPTP + NaB mice, striatal MyD88 levels declined by 44.1% compared to MPTP mice (p < 0.001).
“whereas these levels declined significantly by 45.4%, 44.1%, and 45.9% in the MPTP + NaB mice (p < 0.05, p < 0.001, p < 0.01, respectively) (Figure 7I–L).”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment improved gut microbial dysbiosis in MPTP-induced Parkinson's disease mice.
“According to the results of this study, NaB improved gut microbial dysbiosis and inhibited intestinal inflammation and neuroinflammation, resulting in neuroprotective effects, which involved the TLR4/MyD88/NF-κB pathway.”
Quote in the paperSubstantial claim - Findingown data
NaB treatment suppressed the TLR4/MyD88/NF-kB pathway in the colon and striatum.
“Mechanistic studies revealed that NaB treatment suppressed the TLR4/MyD88/NF-kB pathway in the colon and striatum.”
Quote in the paperSubstantial claim - Findingown data
Verrucomicrobiota abundance was elevated in the PD mice (p < 0.001).
“In terms of the phylum level, Verrucomicrobiota and Proteobacteria were elevated in the PD mice (p < 0.001, p < 0.05, respectively)”
Quote in the paperNot a substantial claim - Findingown data
NaB treatment lowered striatal TNF-α expression by 41.0% compared to MPTP mice (p < 0.01).
“while the NaB treatment considerably lowered the corresponding expression levels by 41.0% and 37.9% (p < 0.01, p < 0.05, respectively) (Figure 7C–E).”
Quote in the paperSubstantial claim - Findingown data
NaB increased striatal neurotransmitter levels in PD mice.
“NaB improved the motor functioning of PD mice, increased striatal neurotransmitter levels, and reduced the death of dopaminergic neurons.”
Quote in the paperSubstantial claim - Findingown data
In MPTP + NaB mice, ZO-1 levels increased by 49.2% compared to MPTP mice (p < 0.05).
“whereas in the MPTP + NaB mice, the occludin and ZO-1 levels increased by 100.5% and 49.2% (p < 0.01 and p < 0.05, respectively) (Figure 6D,E).”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment attenuated MPTP-induced motor symptoms in mice.
“We conducted behavioral experiments on mice and found that NaB treatment attenuated MPTP-induced motor symptoms.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment inhibited the abnormal increase in the abundance of Akkermansia in Parkinson's disease mice.
“Notably, the NaB treatment inhibited the abnormal increase in the abundances of Proteobacteria, Bacteroides, and Akkermansia, which might exert beneficial effects on the PD mice.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment significantly elevated the abundance of Odoribacter in Parkinson's disease mice.
“The abundance of Odoribacter was significantly elevated after the NaB treatment.”
Quote in the paperSubstantial claim - Findingown data
The colonic HE pathology score was remarkably increased in Parkinson's disease mice.
“Herein, we observed a remarkable increase in the colonic HE pathology score in the PD mice, in addition to the elevated expression levels of colonic inflammatory factors, TNF-α and IL-6.”
Quote in the paperSubstantial claim - Findingcitation
Parkinson's disease mice had a higher abundance of Lactobacillus.
“Interestingly, the PD mice had a higher abundance of Lactobacillus, consistent with findings in patients with Crohn’s disease and PD [56,57].”
Quote in the paperNot a substantial claim - Findingreasoning
TLR4/MyD88/NF-kappaB pathway activation was observed in the colon and striatum of Parkinson's disease mice.
“Herein, TLR4/MyD88/NF-B pathway activation was observed in the colon and striatum of the PD mice, possibly due to increased Proteobacteria abundance.”
Quote in the paperSubstantial claim - Findingown data
Parkinson's disease mice showed a significant reduction in Odoribacter abundance.
“The PD mice showed a significant reduction in Odoribacter abundance.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment inhibited TLR4/MyD88/NF-kappaB pathway activation in the colon and striatum of Parkinson's disease mice.
“The NaB treatment, however, inhibited TLR4/MyD88/NF-B pathway activation in the colon and striatum.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate exposure upregulated the expression of ZO-1 and occludin in Parkinson's disease mice.
“In contrast, NaB exposure contributed to upregulated expression of these proteins and restored intestinal barrier function in the PD mice.”
Quote in the paperSubstantial claim - Findingown data
The expression levels of colonic inflammatory factors TNF-alpha and IL-6 were elevated in Parkinson's disease mice.
“Herein, we observed a remarkable increase in the colonic HE pathology score in the PD mice, in addition to the elevated expression levels of colonic inflammatory factors, TNF-α and IL-6.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate exposure restored intestinal barrier function in Parkinson's disease mice.
“In contrast, NaB exposure contributed to upregulated expression of these proteins and restored intestinal barrier function in the PD mice.”
Quote in the paperSubstantial claim - Findingown data
Intestinal permeability was increased in Parkinson's disease mice, as indicated by decreased ZO-1 and occludin levels.
“Our results indicated increased intestinal permeability in the PD mice, as ZO-1 and occludin levels were decreased.”
Quote in the paperSubstantial claim - Findingcitation
The community structure of the gut microbiota in our MPTP-induced Parkinson's disease mouse model changed significantly.
“Consistent with other MPTP-induced PD models [44,45], the community structure of the microbiota in our animal model changed significantly.”
Quote in the paperSubstantial claim - Findingown data
Sodium butyrate treatment suppressed the elevation of TNF-alpha and IL-6 levels in the serum and striatum of Parkinson's disease mice.
“The TNF-α and IL-6 levels were substantially elevated in the serum and striatum, and the NaB treatment suppressed their elevation.”
Quote in the paperSubstantial claim - Findingown data
TNF-alpha and IL-6 levels were substantially elevated in the serum and striatum of Parkinson's disease mice.
“The TNF-α and IL-6 levels were substantially elevated in the serum and striatum, and the NaB treatment suppressed their elevation.”
Quote in the paperSubstantial claim - Premisecitation
The abundance of Akkermansia, Lactobacillus, and Bacteroides genera increased in PD patients.
“the abundance of Akkermansia, Lactobacillus, and Bacteroides genera increased in PD patients, while that of Prevotella, Faecalibacterium, and Roseburia decreased remarkably [8,9,10,11].”
Quote in the paperNot a substantial claim0 of 4 sources checked- cites [8] Jiang, 2017, Impaired endo-lysosomal membrane integrity accelerates the seeding progression of α-synuclein aggregates, Sci. Rep. source
Not checked in the free run.
- cites [9] Lin, 2018, Gut microbiota in patients with Parkinson’s disease in southern China, Parkinsonism Relat. Disord. source
Not checked in the free run.
- cites [10] Sun, 2018, Dysbiosis of gut microbiota and microbial metabolites in Parkinson’s Disease, Ageing Res. Rev. source
Not checked in the free run.
- cites [11] Zheng, 2021, Potential roles of gut microbiota and microbial metabolites in Parkinson’s disease, Ageing Res. Rev. source
Not checked in the free run.
- Premisecitation
Pathological changes in microbial taxonomy have been observed among PD patients.
“Pathological changes in microbial taxonomy have been observed among PD patients.”
Quote in the paperSubstantial claim0 of 4 sources checked- cites [8] Jiang, 2017, Impaired endo-lysosomal membrane integrity accelerates the seeding progression of α-synuclein aggregates, Sci. Rep. source
Not checked in the free run.
- cites [9] Lin, 2018, Gut microbiota in patients with Parkinson’s disease in southern China, Parkinsonism Relat. Disord. source
Not checked in the free run.
- cites [10] Sun, 2018, Dysbiosis of gut microbiota and microbial metabolites in Parkinson’s Disease, Ageing Res. Rev. source
Not checked in the free run.
- cites [11] Zheng, 2021, Potential roles of gut microbiota and microbial metabolites in Parkinson’s disease, Ageing Res. Rev. source
Not checked in the free run.
- Premisecitation
PD pathogenesis may be affected by alterations in the gut microbiota.
“recent studies have demonstrated that PD pathogenesis may be affected by alterations in the gut microbiota [5,6,7].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [5] Sampson, 2016, Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease, Cell source
Not checked in the free run.
- cites [6] Scheperjans, 2015, Gut microbiota are related to Parkinson’s disease and clinical phenotype, Mov. Disord. source
Not checked in the free run.
- cites [7] Cirstea, 2020, Microbiota Composition and Metabolism Are Associated With Gut Function in Parkinson’s Disease, Mov. Disord. source
Not checked in the free run.
- Premisecitation
The abundance of Prevotella, Faecalibacterium, and Roseburia decreased remarkably in PD patients.
“the abundance of Akkermansia, Lactobacillus, and Bacteroides genera increased in PD patients, while that of Prevotella, Faecalibacterium, and Roseburia decreased remarkably [8,9,10,11].”
Quote in the paperSubstantial claim0 of 4 sources checked- cites [8] Jiang, 2017, Impaired endo-lysosomal membrane integrity accelerates the seeding progression of α-synuclein aggregates, Sci. Rep. source
Not checked in the free run.
- cites [9] Lin, 2018, Gut microbiota in patients with Parkinson’s disease in southern China, Parkinsonism Relat. Disord. source
Not checked in the free run.
- cites [10] Sun, 2018, Dysbiosis of gut microbiota and microbial metabolites in Parkinson’s Disease, Ageing Res. Rev. source
Not checked in the free run.
- cites [11] Zheng, 2021, Potential roles of gut microbiota and microbial metabolites in Parkinson’s disease, Ageing Res. Rev. source
Not checked in the free run.
- Interpretationown data
NaB could restore colonic barrier damage in the MPTP mice.
“Taken together, NaB could restore colonic barrier damage in the MPTP mice.”
Quote in the paperSubstantial claim - Interpretationown data
The neuroprotective effects of sodium butyrate in MPTP-induced Parkinson's disease mice involve the TLR4/MyD88/NF-κB pathway.
“According to the results of this study, NaB improved gut microbial dysbiosis and inhibited intestinal inflammation and neuroinflammation, resulting in neuroprotective effects, which involved the TLR4/MyD88/NF-κB pathway.”
Quote in the paperSubstantial claim - Premisecitation
Gut microbiota dysbiosis is associated with the occurrence, development, and progression of Parkinson's disease.
“Growing evidence suggests the association of gut microbiota dysbiosis with PD occurrence, development, and progression [29,30].”
Quote in the paperSubstantial claim0 of 2 sources checked - Interpretationreasoning
Sodium butyrate treatment resulted in neuroprotective effects in MPTP-induced Parkinson's disease mice.
“According to the results of this study, NaB improved gut microbial dysbiosis and inhibited intestinal inflammation and neuroinflammation, resulting in neuroprotective effects, which involved the TLR4/MyD88/NF-κB pathway.”
Quote in the paperSubstantial claim - Premisecitation
The release of pro-inflammatory factors and neurotoxins by activated glial cells leads to neuroinflammation, neuronal damage, and neurodegeneration.
“The release of pro-inflammatory factors and neurotoxins by activated glial cells leads to neuroinflammation, neuronal damage, and neurodegeneration [73].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [73] Miyazaki, I., and Asanuma, M. (2020). Neuron-Astrocyte Interactions in Parkinson’s Disease. Cells, 9. source
Not checked in the free run.
- Premisecitation
Activation of the TLR4/MyD88/NF-kappaB pathway can induce astrocyte and microglial activation.
“Interestingly, activation of the TLR4/MyD88/NF-κB pathway can induce astrocyte and microglial activation [72].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [72] Lucas, 2013, Role of the Toll Like receptor (TLR) radical cycle in chronic inflammation: Possible treatments targeting the TLR4 pathway, Mol. Neurobiol. source
Not checked in the free run.
- Premisecitation
Altered TLR4 signaling contributes to Parkinson's disease pathology.
“Accumulating evidence suggests that altered TLR4 signaling contributes to PD pathology.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [66] Kriz, 2014, Toll-like receptor expression in the blood and brain of patients and a mouse model of Parkinson’s disease, Int. J. Neuropsychopharmacol.
Not checked in the free run.
- cites [67] Dodiya, 2019, Role of TLR4 in the gut-brain axis in Parkinson’s disease: A translational study from men to mice, Gut source
Not checked in the free run.
- Interpretationown data
Sodium butyrate treatment modulated inflammation throughout the gut-brain axis by inhibiting the TLR4/MyD88/NF-kappaB signaling pathway.
“Additionally, the NaB treatment modulated inflammation throughout the gut–brain axis by inhibiting the TLR4/MyD88/NF-kB signaling pathway, a protective mechanism underlying its action.”
Quote in the paperSubstantial claim - Interpretationreasoning
The neuroprotective effect of sodium butyrate on MPTP-induced Parkinson's disease mice may be attributed to the recovery of the composition of the gut microbiota after sodium butyrate treatment.
“In conclusion, the neuroprotective effect of NaB on MPTP-induced PD mice may be attributed to the recovery of the composition of the gut microbiota after NaB treatment.”
Quote in the paperSubstantial claim - Premisecitation
An abnormal increase in pro-inflammatory and other harmful bacteria caused by disorders of the gut microbiota can trigger gut inflammation.
“An abnormal increase in pro-inflammatory and other harmful bacteria caused by disorders of the gut microbiota can trigger gut inflammation [46].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [46] Keshavarzian, 2015, Colonic bacterial composition in Parkinson’s disease, Mov. Disord. source
Not checked in the free run.
- Premisecitation
Toll-like receptors, specifically TLR4, play an instrumental role in intestinal homeostasis.
“Several studies have confirmed that Toll-like receptors, specifically TLR4, play an instrumental role in intestinal homeostasis [65].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [65] Gorecki, 2021, TLR2 and TLR4 in Parkinson’s disease pathogenesis: The environment takes a toll on the gut, Transl. Neurodegener. source
Not checked in the free run.
- Premisecitation
Parkinson's disease patients and animals have increased intestinal permeability.
“PD patients and animals have both been found to have increased intestinal permeability in previous studies [61,62].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [61] Derkinderen, 2019, The Intestinal Barrier in Parkinson’s Disease: Current State of Knowledge, J. Parkinsons Dis. source
Not checked in the free run.
- cites [62] Zhao, 2021, Novel compound FLZ alleviates rotenone-induced PD mouse model by suppressing TLR4/MyD88/NF-B pathway through microbiota-gut-brain axis, Acta. Pharm. Sin. source
Not checked in the free run.
- Premisecitation
Bacteroides abundance correlates with an increase in plasma TNF-alpha and interferon-gamma levels in patients with Parkinson's disease.
“The abundance of Bacteroides also increased significantly in PD mice and is known to correlate with an increase in plasma TNF-α and interferon-γ levels in patients with PD [49].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [49] Bartl, 2022, Evidence for immune system alterations in peripheral biological fluids in Parkinson’s disease, Neurobiol. Dis. source
Not checked in the free run.
- Premisecitation
The Proteobacteria phylum is a marker of dysbiosis in the gut microbiome.
“The Proteobacteria phylum is a marker of dysbiosis in the gut microbiome, and Proteobacteria with pro-inflammatory characteristics are often overexpressed in gastrointestinal and immune diseases [48].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [48] Shin, 2015, Proteobacteria: Microbial signature of dysbiosis in gut microbiota, Trends Biotechnol. source
Not checked in the free run.
- Premisecitation
MPTP-induced Parkinson's disease mice showed attenuation in intestinal inflammation and neuroinflammation upon knocking out of TLR4.
“The MPTP-induced PD mice showed attenuation in intestinal inflammation and neuroinflammation upon the knocking out of TLR4 [67].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [67] Dodiya, 2019, Role of TLR4 in the gut-brain axis in Parkinson’s disease: A translational study from men to mice, Gut source
Not checked in the free run.
- Interpretationreasoning
Sodium butyrate seems to be a potential drug that may be effective at treating Parkinson's disease.
“As a result, NaB seems to be a potential drug that may be effective at treating PD.”
Quote in the paperSubstantial claim
- The quote only partly states this claim. 1
- Classified as probably not a substantial claim. 18
- May combine two claims. 32
The quote only partly states this claim.
Findingown dataIF analysis showed a 51.2% decrease in TH+ dopaminergic neurons in the substantia nigra of PD mice compared to control mice (p < 0.01).
“As shown using IF analysis, a remarkable decrease in TH+ dopaminergic neurons of 51.2% was seen in the PD mice (p < 0.01) compared to the control mice”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Findingown dataMPTP mice tended to have lower striatal DOPAC and 5-HIAA levels than normal mice, but these differences were statistically insignificant.
“The MPTP mice tended to have lower DOPAC and 5-HIAA levels than the normal mice but these differences were statistically insignificant.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataSodium butyrate treatment reduced the gut microbiota's alpha-diversity in Parkinson's disease mice, but the difference was statistically insignificant.
“Although the NaB treatment reduced the α-diversity, the difference was statistically insignificant, suggesting that the sample size needs to be increased in the future.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataNaB mice showed a downward trend in Shannon and Simpson indexes relative to the MPTP group, but this was statistically insignificant.
“The NaB mice showed a downward trend relative to the MPTP group but this was statistically insignificant (Figure 5A,B).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataNaB treatment decreased the abundances of Verrucomicrobiota and Proteobacteria (p > 0.05 for both).
“but the NaB treatment significantly decreased their abundances (p > 0.05, p > 0.05, respectively).”
Quote in the paperSubstantial claimMay combine two claims.
FindingreasoningSodium butyrate treatment inhibited microglial activation and astrocyte activity in Parkinson's disease mice.
“The NaB treatment inhibited microglial activation and astrocyte activity, thus protecting against neuroinflammation and neurodegeneration.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationButyrate exerts anti-inflammatory and anti-oxidant effects while repairing the intestinal barrier.
“Butyrate exerts anti-inflammatory and [18] anti-oxidant effects [19] while repairing the intestinal barrier [20].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [18] Liu, 2019, Sodium Butyrate Inhibits the Inflammation of Lipopolysaccharide-Induced Acute Lung Injury in Mice by Regulating the Toll-Like Receptor 4/Nuclear Factor κB Signaling Pathway, J. Agric. Food Chem. source
Not checked in the free run.
- cites [19] Zhao, J., Hu, J., and Ma, X. (2021). Sodium Decanoate Improves Intestinal Epithelial Barrier and Antioxidation via Activating G Protein-Coupled Receptor-43. Nutrients, 13. source
Not checked in the free run.
- cites [20] Chen, 2018, Sodium Butyrate Inhibits Inflammation and Maintains Epithelium Barrier Integrity in a TNBS-induced Inflammatory Bowel Disease Mice Model, EBioMedicine source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationNaB reduced the entry of inflammatory factors into the liver by regulating gut microbial dysbiosis, thereby reducing steatohepatitis induced by a high-fat diet.
“Zhou et al. reported that sodium butyrate (NaB) reduced the entry of inflammatory factors into the liver by regulating gut microbial dysbiosis, thereby reducing steatohepatitis induced by a high-fat diet [21].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [21] Zhou, 2017, Sodium butyrate attenuates high-fat diet-induced steatohepatitis in mice by improving gut microbiota and gastrointestinal barrier, World J. Gastroenterol. source
Not checked in the free run.
May combine two claims.
PremisecitationNaB can improve motor symptoms, neuronal loss, and neuroinflammation in MPTP-induced PD mice.
“NaB can improve motor symptoms, neuronal loss, and neuroinflammation in MPTP-induced PD mice [23,24,25].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [23] Hou, 2021, Neuroprotective effects of short-chain fatty acids in MPTP induced mice model of Parkinson’s disease, Exp. Gerontol. source
Not checked in the free run.
- cites [24] Sharma, 2015, Beneficial effects of sodium butyrate in 6-OHDA induced neurotoxicity and behavioral abnormalities: Modulation of histone deacetylase activity, Behav. Brain Res. source
Not checked in the free run.
- cites [25] Liu, 2017, Sodium butyrate exerts protective effect against Parkinson’s disease in mice via stimulation of glucagon like peptide-1, J. Neurol. Sci. source
Not checked in the free run.
May combine two claims.
Interpretationown dataNaB could improve locomotor functions and exploratory behaviors in the PD mice.
“These results demonstrated that NaB could improve locomotor functions and exploratory behaviors in the PD mice.”
- Also stated in: § Abstract · plain
“NaB improved the motor functioning of PD mice”
Quote in the paperSubstantial claim- Also stated in: § Abstract · plain
Classified as probably not a substantial claim.
PremisecitationDopaminergic neuron loss in the substantia nigra along with a decline in dopamine released to the striatum constitutes the pathological PD hallmark.
“Dopaminergic neuron loss in the substantia nigra along with a decline in dopamine (DA) released to the striatum constitutes the pathological PD hallmark [3].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [3] Poewe, 2017, Parkinson disease, Nat. Rev. Dis. Primers source
Not checked in the free run.
May combine two claims.
PremisecitationFeces of patients with PD transplanted in germ-free mice showed severe motor impairments, inflammation, and other pathological symptoms.
“the feces of patients with PD transplanted in germ-free mice showed severe motor impairments, inflammation, and other pathological symptoms [12].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [12] Zhao, 2021, Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis, Microbiome source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe MPTP mouse model was created using a previously reported technique.
“To create the MPTP mouse model, we applied a technique that was previously reported [25,26].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [25] Liu, 2017, Sodium butyrate exerts protective effect against Parkinson’s disease in mice via stimulation of glucagon like peptide-1, J. Neurol. Sci. source
Not checked in the free run.
- cites [26] Sun, 2021, Probiotic Clostridium butyricum ameliorated motor deficits in a mouse model of Parkinson’s disease via gut microbiota-GLP-1 pathway, Brain Behav. Immun. source
Not checked in the free run.
May combine two claims.
Interpretationown dataNaB performed a neuroprotective function in the PD mice by increasing striatal TH expression and restoring dopaminergic neuron loss.
“The above results suggested that NaB performed a neuroprotective function in the PD mice by increasing striatal TH expression and restoring dopaminergic neuron loss.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationIncreased Bacteroides abundance in PD patients correlated positively with the severity of their motor disorders.
“Lin et al. reported that increased Bacteroides abundance in PD patients correlated positively with the severity of their motor disorders [9].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [9] Lin, 2018, Gut microbiota in patients with Parkinson’s disease in southern China, Parkinsonism Relat. Disord. source
Not checked in the free run.
May combine two claims.
PremisecitationGut microbial dysbiosis leads to intestinal inflammation and increases intestinal permeability.
“gut microbial dysbiosis not only leads to intestinal inflammation but also increases intestinal permeability.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [14] Wang, 2021, The role of gut dysbiosis in Parkinson’s disease: Mechanistic insights and therapeutic options, Brain source
Not checked in the free run.
- cites [15] Zhu, 2022, Gut Microbiota: A Novel Therapeutic Target for Parkinson’s Disease, Front. Immunol. source
Not checked in the free run.
- cites [16] Chidambaram, 2022, Gut dysbiosis, defective autophagy and altered immune responses in neurodegenerative diseases: Tales of a vicious cycle, Pharmacol. Ther. source
Not checked in the free run.
Classified as probably not a substantial claim.
Study design and conductnone givenMice were randomly classified into three groups (control, MPTP, MPTP+NaB) with n=12 per group.
“Mice were randomly classified (n = 12 per group) into the three following groups: control; MPTP; and MPTP + NaB groups.”
Quote in the paperSubstantial claimMay combine two claims.
PremisereasoningRemodeling the gut microbiota to reduce intestinal permeability and inhibiting intestinal inflammation to reduce neuroinflammation and elicit neuroprotective effects in PD may be a promising treatment strategy.
“Hence, remodeling the gut microbiota to reduce intestinal permeability and inhibiting intestinal inflammation to reduce neuroinflammation and elicit neuroprotective effects in PD may be a promising treatment strategy for these patients.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationButyrate is a short-chain fatty acid synthesized by anaerobes in the colon of animals through fermentation of indigestible dietary fibers.
“Butyrate is a short-chain fatty acid (SCFA) synthesized by anaerobes in the colon of animals through the fermentation of indigestible dietary fibers [17].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [17] Serena, 2003, New insight into butyrate metabolism, Proc. Nutr. Soc. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationColon pathology was scored according to previously described criteria.
“which were subjected to the HE staining protocol and scored pathologically according to previously described criteria [27].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [27] Lee, 2016, The vitamin D receptor functions as a transcription regulator in the absence of 1,25-dihydroxyvitamin D, J. Steroid Biochem. Mol. Biol. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationNaB regulated gut microbial composition, specifically reducing harmful bacteria and increasing beneficial bacteria, in mice with liver metastasis of colon cancer.
“Ma et al. found that NaB regulated gut microbial composition, specifically reducing harmful bacteria and increasing beneficial bacteria, in mice with liver metastasis of colon cancer [22].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [22] Ma, 2020, Sodium butyrate modulates gut microbiota and immune response in colorectal cancer liver metastatic mice, Cell Biol. Toxicol. source
Not checked in the free run.
May combine two claims.
Interpretationown dataNaB prevented neurodegeneration in the PD mice by attenuating inflammation of the entire gut-brain axis, which might be achieved by targeting the gut microbiota, and also involved the TLR4/MyD88/NF-κB pathway.
“Our results suggested that NaB prevented neurodegeneration in the PD mice by attenuating inflammation of the entire gut–brain axis, which might be achieved by targeting the gut microbiota, and also involved the TLR4/MyD88/NF-κB pathway.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim. May combine two claims.
PremisecitationNeuroinflammation is an important pathophysiological feature of PD and is associated with neurodegeneration.
“Neuroinflammation is regarded as an important pathophysiological feature of PD, which is associated with neurodegeneration [4].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [4] Hirsch, 2009, Neuroinflammation in Parkinson’s disease: A target for neuroprotection?, Lancet Neurol. source
Not checked in the free run.
May combine two claims.
PremisecitationTransplanting healthy donor gut microbiota into mice with MPTP-induced PD substantially improved bodily injuries and exerted a neuroprotective effect.
“Sun et al. found that transplanting healthy donor gut microbiota into mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD substantially improved the bodily injuries in these recipient mice and exerted a neuroprotective effect [13].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [13] Sun, 2018, Neuroprotective effects of fecal microbiota transplantation on MPTP-induced Parkinson’s disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behav. Immun. source
Not checked in the free run.
May combine two claims.
PremisecitationAltering the gut microbiota composition is a viable target for diagnosing and treating Parkinson's disease.
“Altering the gut microbiota composition is a viable target for diagnosing and treating PD [31,32].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [31] Fan, 2022, New hope for Parkinson’s disease treatment: Targeting gut microbiota, CNS Neurosci. Ther. source
Not checked in the free run.
- cites [32] Varesi, A., Campagnoli, L.I.M., Fahmideh, F., Pierella, E., Romeo, M., Ricevuti, G., Nicoletta, M., Chirumbolo, S., and Pascale, A. (2022). The Interplay between Gut Microbiota and Parkinson’s Disease: Implications on Diagnosis and Treatment. Int. J. Mol. Sci., 23. source
Not checked in the free run.
May combine two claims.
Interpretationown dataNaB treatment inhibited glial cell activation, leading to reduced neuroinflammation.
“Thus, the NaB treatment inhibited glial cell activation, leading to reduced neuroinflammation.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataThe control and MPTP mice were separated in beta diversity, with the NaB treatment group located in between the two groups, suggesting that NaB treatment shifted the overall MPTP-damaged gut microbiota composition towards that of the control group.
“Moreover, the results demonstrated that the control and MPTP mice were separated, with the NaB treatment group located in between the two groups, suggesting that the NaB treatment shifted the overall MPTP-damaged gut microbiota composition towards that of the control group.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataNaB had a neuroprotective impact on the PD mice, likely linked to its regulation of gut microbiota to inhibit gut-brain axis inflammation.
“In summary, NaB had a neuroprotective impact on the PD mice, likely linked to its regulation of gut microbiota to inhibit gut–brain axis inflammation.”
Quote in the paperSubstantial claim- Rests on an assumption: The specific mechanism behind the neuroprotective properties of NaB against PD is mostly obscure.
May combine two claims.
PremisecitationSodium butyrate exerts anti-apoptotic, anti-inflammatory, and neuroprotective effects on mice with Parkinson's disease.
“Notably, NaB exerts anti-apoptotic, anti-inflammatory, and neuroprotective effects on mice with PD [36,37,38]”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [36] Kakoty, 2021, Neuroprotective Effects of Trehalose and Sodium Butyrate on Preformed Fibrillar Form of α-Synuclein-Induced Rat Model of Parkinson’s Disease, ACS Chem. Neurosci. source
Not checked in the free run.
- cites [37] Paiva, 2017, Sodium butyrate rescues dopaminergic cells from alpha-synuclein-induced transcriptional deregulation and DNA damage, Hum. Mol. Genet. source
Not checked in the free run.
- cites [38] Zhang, 2022, Sodium butyrate attenuates rotenone-induced toxicity by activation of autophagy through epigenetically regulating PGC-1α expression in PC12 cells, Brain Res. source
Not checked in the free run.
May combine two claims.
Interpretationown dataMPTP-induced mice had gut microbial dysbiosis, and NaB treatment improved gut dysbiosis in these animals by modulating microbiota composition.
“The data suggested that the MPTP-induced mice had gut microbial dysbiosis, and that the NaB treatment improved gut dysbiosis in these animals by modulating microbiota composition.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataNaB reduced intestinal inflammation and neuroinflammation by suppressing the activities of the TLR4/MyD88/NF-κB signaling pathway.
“Thus, NaB reduced intestinal inflammation and neuroinflammation by suppressing the activities of the TLR4/MyD88/NF-κB signaling pathway.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationSodium butyrate treatment has no significant effect on normal animals, including on gut microbiota, intestinal inflammation, neuroinflammation, and motor function.
“The NaB treatment had no significant effect on normal animals, especially on gut microbiota [22], intestinal inflammation [33], neuroinflammation [34], and motor function [35].”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [22] Ma, 2020, Sodium butyrate modulates gut microbiota and immune response in colorectal cancer liver metastatic mice, Cell Biol. Toxicol. source
Not checked in the free run.
- cites [33] Vieira, 2012, Oral administration of sodium butyrate attenuates inflammation and mucosal lesion in experimental acute ulcerative colitis, J. Nutr. Biochem. source
Not checked in the free run.
- cites [34] Jaworska, 2017, The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia, J. Neuroinflamm. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationProteobacteria with pro-inflammatory characteristics are often overexpressed in gastrointestinal and immune diseases.
“The Proteobacteria phylum is a marker of dysbiosis in the gut microbiome, and Proteobacteria with pro-inflammatory characteristics are often overexpressed in gastrointestinal and immune diseases [48].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [48] Shin, 2015, Proteobacteria: Microbial signature of dysbiosis in gut microbiota, Trends Biotechnol. source
Not checked in the free run.
May combine two claims.
PremisecitationAkkermansia can degrade mucin, cause intestinal inflammation and permeability, and increase endotoxemia and systemic inflammation, eventually promoting neuropathology.
“The Gram-negative bacteria, Akkermansia, can degrade mucin, cause intestinal inflammation and permeability, and increase endotoxemia and systemic inflammation, eventually promoting neuropathology [53,54,55].”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [53] Freedman, 2018, The "Gut Feeling": Breaking Down the Role of Gut Microbiome in Multiple Sclerosis, Neurotherapeutics source
Not checked in the free run.
- cites [54] Desai, 2016, A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility, Cell source
Not checked in the free run.
- cites [55] Ganesh, B.P., Klopfleisch, R., Loh, G., and Blaut, M. (2013). Commensal Akkermansia muciniphila exacerbates gut inflammation in Salmonella Typhimurium-infected gnotobiotic mice. PLoS ONE, 8. source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationPreservation of the intestinal barrier's integrity relies on the tight junctions between intestinal epithelial cells and their molecular structure including ZO and occludin.
“The preservation of the intestinal barrier’s integrity relies on the tight junctions between intestinal epithelial cells and their molecular structure including the cytoplasmic and transmembrane proteins, ZO, and occludin [63].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [63] Salama, 2006, Tight junction modulation and its relationship to drug delivery, Adv. Drug Deliv. Rev. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe motor symptoms of Parkinson's disease may result from decreased dopamine and serotonin levels.
“The motor symptoms of PD may result from decreased dopamine and serotonin levels [41,42].”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
PremisecitationInflammatory LPS is produced by abnormally high Proteobacteria, and TLR4 recognizes elevated inflammatory LPS, in turn activating the MyD88-dependent NF-kappaB signaling pathway.
“Inflammatory LPS is produced by abnormally high Proteobacteria, and TLR4 recognizes elevated inflammatory LPS [69], in turn activating the MyD88-dependent NF-κB signaling pathway.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [69] Lin, 2020, Like Cures Like: Pharmacological Activity of Anti-Inflammatory Lipopolysaccharides From Gut Microbiome, Front. Pharmacol. source
Not checked in the free run.
Classified as probably not a substantial claim. May combine two claims.
PremisecitationTH downregulation decreases DA production, in turn leading to Parkinson's disease.
“TH downregulation decreases DA production, in turn leading to PD [39].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [39] Haavik, 1998, Tyrosine hydroxylase and Parkinson’s disease, Mol. Neurobiol. source
Not checked in the free run.
May combine two claims.
PremisecitationTNF-alpha and IL-6 are downstream products of NF-kappaB, so when the TLR4 pathway is activated, they are produced more readily.
“TNF-α and IL-6 are downstream products of NF-KB, so when the TLR4 pathway is activated, they are produced more readily [70,71].”
Quote in the paperSubstantial claim0 of 2 sources checkedProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe content of 5-HT decreases in mouse models of Parkinson's disease.
“The content of 5-HT reportedly decreases in mouse models of PD [13,40].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [13] Sun, 2018, Neuroprotective effects of fecal microbiota transplantation on MPTP-induced Parkinson’s disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behav. Immun. source
Not checked in the free run.
- cites [40] Dong, 2020, Polymannuronic acid prevents dopaminergic neuronal loss via brain-gut-microbiota axis in Parkinson’s disease model, Int. J. Biol. Macromol. source
Not checked in the free run.
May combine two claims.
PremisecitationDue to increased intestinal permeability, microbial toxins and pro-inflammatory mediators produced as a result of gut dysbiosis can leak into the circulation causing systemic inflammation, in turn destroying the blood-brain barrier and causing neuroinflammation.
“Due to increased intestinal permeability, microbial toxins and pro-inflammatory mediators produced as a result of gut dysbiosis can leak into the circulation causing systemic inflammation, in turn destroying the blood–brain barrier and causing neuroinflammation [12,64].”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [12] Zhao, 2021, Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis, Microbiome source
Not checked in the free run.
- cites [64] Pavlov, 2015, Neural circuitry and immunity, Immunol. Res. source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationGut inflammation increases intestinal permeability.
“According to the popular “leaky gut” theory, gut inflammation increases intestinal permeability [60].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [60] Metta, 2022, Gastrointestinal dysfunction in Parkinson’s disease: Molecular pathology and implications of gut microbiome, probiotics, and fecal microbiota transplantation, J. Neurol. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSodium butyrate treatment ameliorates motor symptoms in a Drosophila rotenone-induced Parkinson's disease model.
“The NaB treatment ameliorates motor symptoms in a Drosophila rotenone-induced PD model [43].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [43] Ahmad, 2013, Sodium butyrate improves locomotor impairment and early mortality in a rotenone-induced Drosophila model of Parkinson’s disease, Neuroscience source
Not checked in the free run.
May combine two claims.
PremisecitationPatients with Parkinson's disease show elevated TLR4 protein levels in their colonic biopsies, circulating monocytes, as well as postmortem caudate and putamen samples.
“For instance, patients with PD show elevated TLR4 protein levels in their colonic biopsies, circulating monocytes, as well as postmortem caudate and putamen samples [66,67].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [66] Kriz, 2014, Toll-like receptor expression in the blood and brain of patients and a mouse model of Parkinson’s disease, Int. J. Neuropsychopharmacol.
Not checked in the free run.
- cites [67] Dodiya, 2019, Role of TLR4 in the gut-brain axis in Parkinson’s disease: A translational study from men to mice, Gut source
Not checked in the free run.
May combine two claims.
PremisecitationBoth mice and patients with Parkinson's disease exhibit increased levels of the genus Akkermansia.
“Both mice and patients with PD exhibit increased levels of the genus Akkermansia [51,52].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [51] Zhou, 2021, Neuroprotective Effect of Ceftriaxone on MPTP-Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota, Oxid. Med. Cell. Longev. source
Not checked in the free run.
- cites [52] Menozzi, 2021, The gut-brain axis and Parkinson disease: Clinical and pathogenetic relevance, Ann. Med. source
Not checked in the free run.
May combine two claims.
PremisecitationOdoribacter is a beneficial bacterium known for producing short-chain fatty acids and reducing inflammation.
“Odoribacter is a beneficial bacteria known for producing SCFAs and reducing inflammation [59].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [59] Bellido, 2019, Effect of Synbiotic Supplementation in a Very-Low-Calorie Ketogenic Diet on Weight Loss Achievement and Gut Microbiota: A Randomized Controlled Pilot Study, Mol. Nutr. Food Res. source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe TLR4/MyD88/NF-kappaB pathway is well recognized for its role in the inflammatory signaling pathway.
“The TLR4/MyD88/NF-κB pathway is well recognized for its role in the inflammatory signaling pathway [68].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [68] Rahimifard, 2017, Targeting the TLR4 signaling pathway by polyphenols: A novel therapeutic strategy for neuroinflammation, Ageing Res. Rev. source
Not checked in the free run.
May combine two claims.
InterpretationreasoningSodium butyrate treatment reduced MPTP-induced inflammation in the gut-brain axis of Parkinson's disease mice, which might be associated with the TLR4/MyD88/NF-kappaB signaling pathway.
“Based on these results, the NaB treatment reduced MPTP-induced inflammation in the gut–brain axis of the PD mice, which might be associated with the TLR4/MyD88/NF-B signaling pathway.”
Quote in the paperSubstantial claim
The paper relies on this without support.
The specific mechanism behind the neuroprotective properties of NaB against PD is mostly obscure.
“Nevertheless, the specific mechanism behind the neuroprotective properties of NaB against PD is mostly obscure.”
The paper relies on this without support.
Current treatments for PD can alleviate symptoms but cannot prevent neurodegeneration.
“Although current treatments can alleviate PD symptoms, they are not able to prevent its neurodegeneration.”
The authors state this as an assumption.
The exact mechanism underlying the effects of sodium butyrate in Parkinson's disease remains unclear.
“but the exact mechanism underlying these effects of NaB in PD remains unclear.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Sodium butyrate has neuroprotective effects in MPTP-induced PD mice by attenuating microglial reactivity via inhibition of TLR4/MyD88/NF-κB and MAPK signaling pathway.
“Additionally, studies have demonstrated the neuroprotective effects of sodium butyrate in MPTP-induced PD mice by attenuating microglial reactivity via the inhibition of TLR4/MyD88/NF-κB and MAPK signaling pathway.319–321”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [320]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Striatal cytokines are reported as both decreased and elevated in PD mice
MajorThe results report lower striatal TNF-α and IL-6 in MPTP mice, but the discussion states that both were substantially elevated in the striatum.
“The Western blotting illustrated a substantial decline in the levels of TNF-α and IL-6 of 78.7% and 55.1%, respectively, in the striatum of the MPTP mice (p < 0.01, p < 0.05)”
“The TNF-α and IL-6 levels were substantially elevated in the serum and striatum, and the NaB treatment suppressed their elevation.”
GFAP results do not show MPTP-induced astrocyte activation
MajorGFAP, the stated astrocyte marker, decreased in MPTP mice and decreased further with NaB. This conflicts with the section's characterization of NaB as attenuating MPTP-induced astrocyte activation.
“The MPTP mice displayed a 53.6% decrease in GFAP expression compared to the control mice in the striatum (p < 0.001). The treatment with NaB decreased GFAP expression (p < 0.01) by 26.2% in the MPTP mice (Figure 4B,C).”
“### 3.4. NaB in Mice with MPTP-Induced PD Attenuates Microglia and Astrocyte Activation”
Nonsignificant microbiota changes are called significant
MinorThe text calls both NaB-associated decreases significant despite reporting p > 0.05 for each, whereas the paper defines significance as p < 0.05.
“In terms of the phylum level, Verrucomicrobiota and Proteobacteria were elevated in the PD mice (p < 0.001, p < 0.05, respectively) but the NaB treatment significantly decreased their abundances (p > 0.05, p > 0.05, respectively).”
“A value of p < 0.05 indicated the significance criterion.”
Colonic pathway proteins are reported as decreased despite a claim of activation
MinorThe results say colonic TLR4, MyD88, and NF-B protein expression decreased in PD mice, while the discussion says the pathway was activated in their colons.
“Similarly, TLR4, MyD88, and NF-B protein expression decreased nearly 70%, 94.7%, and 94.2% in the colons of the PD group mice, respectively (p < 0.01, p < 0.05, p < 0.05, respectively).”
“Herein, TLR4/MyD88/NF-B pathway activation was observed in the colon and striatum of the PD mice, possibly due to increased Proteobacteria abundance.”
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Self-citationNew insight into butyrate metabolism
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Potential roles of gut microbiota and microbial metabolites in Parkinson’s disease
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Self-citationNeuroprotective effects of short-chain fatty acids in MPTP induced mice model of Parkinson's disease
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The Intestinal Barrier in Parkinson’s Disease: Current State of Knowledge
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Microbiome changes: an indicator of Parkinson’s disease?
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The gut-brain axis and Parkinson disease: Clinical and pathogenetic relevance
Menozzi, E., Macnaughtan, J., & Schapira, A. H. V. (2021) · Annals of Medicine · doi:10.1080/07853890.2021.1890330 · Cited by 81 · see citing works
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New hope for Parkinson’s disease treatment: Targeting gut microbiota
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Evidence for immune system alterations in peripheral biological fluids in Parkinson’s disease
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Dysfunction of serotonergic neurons in Parkinson’s disease and dyskinesia
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
Loh, J. S., Mak, W. Q., Tan, L. K. S., Ng, C. X., Chan, H. H., Yeow, S. H., Foo, J. B., Ong, Y. S., How, C. W., & Khaw, K. Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01743-1 · Cited by 1,193 · see citing works
Gut microbiota-derived short-chain fatty acids and their role in human health and disease
Mukhopadhya, I., & Louis, P. (2025) · Nature Reviews Microbiology · doi:10.1038/s41579-025-01183-w · Cited by 586 · see citing works
“Butyrate and propionate supplementation has been shown to exert a protective effect against Parkinson disease development in mice 166,167 .”
Li, Y., Liu, A., Chen, K., Li, L., Zhang, X., Zou, F., Zhang, X., & Meng, X. (2024) · Environment International · doi:10.1016/j.envint.2024.108479 · Cited by 91 · see citing works
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Self-citationGut Microbiota as an Endocrine Organ: Unveiling Its Role in Human Physiology and Health
Pires, L., Paramás, A. M. G., Heleno, S. A., & Calhelha, R. C. (2024) · Applied Sciences · doi:10.3390/app14209383 · Cited by 87 · see citing works
“…is of particular interest in comprehending the influence of gut microbes on neurodegenerative disorders characterised by dopaminergic neuron degeneration, such as PD. Propionate, another SCFA produced by Bacteroidetes and Firmicutes , has also been associated with gut–brain communication [101].”
Dothel, G., Barbaro, M. R., Vito, A. D., Ravegnini, G., Gorini, F., Monesmith, S., Coschina, E., Benuzzi, E., Fuschi, D., Palombo, M., et al. (2023) · Journal of Gastroenterology · doi:10.1007/s00535-023-01997-6 · Cited by 46 · see citing works
“Still at a central level, akin results showed improved neuromotor capabilities of mice models of Parkinson’s Disease treated with SB, linking this effect to an inhibition of the TLR4/MyD88/NF-B inflammatory pathway, as well as to a beneficial effect on intestinal barrier elicited by a reduction of dysbiosis [102].”
BackgroundResultSun, J., Lu, L., Lian, Y., Xu, S., Zhu, Y., Wu, Y., Lin, Q., Hou, J., Li, Y., & Yu, Z. (2025) · Molecular Brain · doi:10.1186/s13041-025-01179-w · Cited by 50 · see citing works
“A recent study demonstrated that in Parkinson’s disease, SB improves brain function by inhibiting microglia-mediated neuroinflammation by TLR4/MyD88/NF-κB signaling pathway [36].”
Uceda, S., Echeverry‐Alzate, V., Reiriz, M., Miguel, E. M., Pérez-Curiel, A., Gómez-Senent, S., & Beltrán-Velasco, A. I. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713294 · Cited by 35 · see citing works
“In addition, we now know that the certain markers of the pathology are related to an increase in intestinal permeability, called leaky gut syndrome [58].”
BackgroundThe Gut Microbiome-Neuroglia Axis: Implications for Brain Health, Inflammation, and Disease
Camberos-Barraza, J., Guadrón‐Llanos, A. M., & la Herrán-Arita, A. K. D. (2024) · Neuroglia · doi:10.3390/neuroglia5030018 · Cited by 34 · see citing works
“SCFAs, such as butyrate, have neuroprotective effects and can modulate brain inflammation and neurogenesis [51,52].”
BackgroundSoni, D., Upadhayay, S., Dhureja, M., Arthur, R., & Kumar, P. (2024) · Inflammopharmacology · doi:10.1007/s10787-024-01510-2 · Cited by 31 · see citing works
“Various studies reported that the treatment of compounds includes chicorin acid (Wang et al. 2022), sodium butyrate (Guo et al. 2023), Dihuang Granule (He et al. 2023), Nardostachys jatamansi oil (Wan et al. 2022), polymannuronic acid (Dong et al. 2020), and a novel compound FLZ (Zhao et al. 2021a,…”
Zhang, W., Ding, L., Zhang, M., Zheng, S., Ma, R., Gong, J., Mao, H., Xu, H., Xu, P., & Zhang, Y. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04807-7 · Cited by 29 · see citing works
“Mechanistically, butyrate could inhibit TLR4/MyD88/NF-κB pathway in the colon and striatum, and suppress the production of proinflammatory cytokines [68, 69].”
BackgroundQu, Y., An, K., Wang, D., Yu, H., Li, J., Min, Z., Xiong, Y., Xue, Z., & Mao, Z. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-04726-7 · Cited by 30 · see citing works
Nicese, M. N., Bijkerk, R., van Zonneveld, A. J., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713090 · Cited by 25 · see citing works
“Interestingly, the benefits of butyrate also go beyond the cardiovascular system, as they have been observed for instance acting on the central nervous system [52] and on intestinal barrier integrity [53,54].”
BackgroundThe link between the gut microbiome, inflammation, and Parkinson’s disease
Nie, S., & Ge, Y. (2023) · Applied Microbiology and Biotechnology · doi:10.1007/s00253-023-12789-6 · Cited by 23 · see citing works
“Sodium butyrate exerted neuroprotective effects in PD mice by restoring gut microbiota and inhibiting Toll-like receptor 4 (TLR4) signaling (Guo et al. 2023).”
BackgroundThe interplay between gut microbiota and the brain-gut axis in Parkinson’s disease treatment
Jia, X., Wang, Q., Liu, M., & Ding, J.-Y. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1415463 · Cited by 24 · see citing works
Zhu, W., Hu, Y., Shi, Y., Bao, H., Cheng, X., Jiang, M., Peng, Z., Song, J., Fang, F., Jian, C., et al. (2025) · Microbiological Research · doi:10.1016/j.micres.2025.128077 · Cited by 24 · see citing works
Buty and the beast: the complex role of butyrate in Parkinson’s disease
Elford, J. D., Becht, N. N., Garssen, J., Kraneveld, A. D., & Perez‐Pardo, P. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1388401 · Cited by 27 · see citing works
Kumar, D., Bishnoi, M., Kondepudi, K. K., & Sharma, S. S. (2025) · Probiotics and Antimicrobial Proteins · doi:10.1007/s12602-024-10433-x · Cited by 21 · see citing works
Araújo, L. P., Godoy, A. C. F., Frota, F. F., Lamas, C. B., Quesada, K. R., Detregiachi, C. R. P., Araújo, A. C., Miglino, M. A., Guiguer, É. L., Haber, R. S. D. A., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262412147 · Cited by 30 · see citing works
“This key metabolite maintains intestinal barrier integrity and exerts anti-inflammatory and neuroprotective effects [220].”
Duan, W.-X., Xie, W.-Y., Ying, C., Fen, W., Cheng, X.-Y., Mao, C.-J., Liu, J., & Liu, C.-F. (2025) · npj Parkinson s Disease · doi:10.1038/s41531-025-01029-5 · Cited by 21 · see citing works
“To verify whether the improvement in sleep disorders caused by butyrate in PD patients is related to changes in dopamine transmitters or receptors 25,26 , we conducted studies using madopar for dopamine replacement therapy and pramipexole for dopamine receptor agonist therapy to…”
Rojo, N. D., Blanco-Benítez, M., Cava, R., Fuentes, J. M., Canales-Cortés, S., & González‐Polo, R. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252111629 · Cited by 17 · see citing works
“Similar results were observed with NaB [24], CDG [25], OFO [27], and GEP [26].”
ResultMissiego-Beltrán, J., Olalla-Álvarez, E. M., González-Brugera, A., & Beltrán-Velasco, A. I. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25168998 · Cited by 18 · see citing works
“Guo et al. (2023) conducted a study to evaluate the neuroprotective effects of NaB in a male C57BL/6 mouse model of MPTP-induced PD.”
BackgroundRosell‐Cardona, C., Leigh, S., Knox, E. G., Tirelli, E., Lyte, J. M., Goodson, M. S., Kelley‐Loughnane, N., Aburto, M. R., Cryan, J. F., & Clarke, G. A. (2025) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2025.100992 · Cited by 18 · see citing works
Xu, Y., Wen, L., Tang, Y., Zhao, Z., Xu, M., Wang, T., & Chen, Z. (2024) · Immunity Inflammation and Disease · doi:10.1002/iid3.1194 · Cited by 13 · see citing works
“44 – 47 In this study, we have explored the underlying mechanisms by which NaB exerts protective effects against PD ‐ like conditions.”
BackgroundNohesara, S., Abdolmaleky, H. M., Pirani, A., & Thiagalingam, S. (2025) · Cells · doi:10.3390/cells14131027 · Cited by 14 · see citing works
“In another clinical study conducted by Schweickart et al., the Mediterranean KD was capable of alleviating risk factors of AD by decreasing the inflammatory marker GlycA, suggesting a reduction in systemic inflammation owing to the effects of this type diet [192].”
Hajare, S., & Kulkarni, Y. A. (2025) · Brain Research · doi:10.1016/j.brainres.2025.149975 · Cited by 16 · see citing works
Chen, M., Zhang, Y., Hou, L., Zhao, Z., Tang, P., Sun, Q., Zhao, J., & Wang, Q. (2025) · npj Parkinson s Disease · doi:10.1038/s41531-025-00892-6 · Cited by 15 · see citing works
“Similarly, other neuroprotective drugs, such as Eucommiae and Sodium Butyrate, can also mitigate the disruption of the intestinal barrier and inhibit in fl ammation 34,35 .”
Protective Effects of Bifidobacterium Breve MCC1274 as a Novel Therapy for Alzheimer’s Disease
Abdelhamid, M., Counts, S., Zhou, C., Hida, H., Kim, J., Michikawa, M., & Jung, C. (2025) · Nutrients · doi:10.3390/nu17030558 · Cited by 16 · see citing works
“Additionally, butyrate has been shown to exert anti-inflammatory effects and promote neurogenesis [52].”
Perspective on alcohol-induced organ damage via autophagy-dependent cellular changes
Bakheet, A., Anbazhagan, M., Barve, S. S., Dasarathy, S., Dickinson, J. J., Ding, W., Donohue, T. M., Gopal, T., Gukovskaya, A. S., Kharbanda, K. K., et al. (2025) · Redox Biology · doi:10.1016/j.redox.2025.103879 · Cited by 16 · see citing works
“In Parkinson ’ s disease models, NaB restored gut homeostasis and reduced microglial activation [247].”
Mehboodi, M., Namdari, M. P., Abdollahi, Z., Mobarezi, Z., Kiani, M., Chamani, F., Khanbabaie, H., Rabiei, S., Maleki, M. H., Sanati, H., et al. (2025) · Microbial Pathogenesis · doi:10.1016/j.micpath.2025.107905 · Cited by 14 · see citing works
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Frataxin deficiency shifts metabolism to promote reactive microglia via glucose catabolism
Sciarretta, F., Zaccaria, F., Ninni, A., Ceci, V., Turchi, R., Apolloni, S., Milani, M., Valle, I. D., Tiberi, M., Chiurchiù, V., et al. (2024) · Life Science Alliance · doi:10.26508/lsa.202402609 · Cited by 13 · see citing works
“Butyrate had a neuroprotective impact on mouse models of Parkinson ’ s disease, likely due to the downstream regulation of gut microbiota and inhibition of gut – brain axis in-fl ammation (Guo et al, 2023).”
The Intricate Interplay: Microbial Metabolites and the Gut‐Liver‐Brain Axis in Parkinson's Disease
Kishanchand, D. K., A., A. K. K., Chandrababu, K., Philips, C. A., Sivan, U., & Chakrapani, P. S. B. (2025) · Journal of Neuroscience Research · doi:10.1002/jnr.70016 · Cited by 11 · see citing works
“The TLR4/MyD88/NF-κB pathway mediated these protective effects (Guo et al. 2023).”
The role of the gut microbiota in neuropsychiatric disorders and therapy
Zhang, F., Ding, K., Zhang, L., Liu, D., Dong, X., Wang, M., Zhou, F.-L., Sun, Y., Zhang, W., Yu, Y., et al. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102894 · Cited by 11 · see citing works
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Cui, Y., Cen, Q., Feng, J., Wei, J., Wang, L., Chang, C., Pang, R., Wang, J., & Zhang, A. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01589-8 · Cited by 9 · see citing works
“Guo et al.(Guo et al. 2023) found that NaB improved motor function, increased stria - tal neurotransmitter levels, reduced dopaminergic neuron death, and restored disturbed gut microbiota in Parkinson’s mice.”
Therapeutic Potential of Sodium Butyrate in Neurological and Psychiatric Disorders
Rahmani, D., Chodari, L., Kakallahpour, M., & Niknam, Z. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05428-w · Cited by 9 · see citing works
Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases
Olajide, T. S., & Ijomone, O. M. (2025) · Neuroprotection/Neuroprotection (Chichester, England. Print) · doi:10.1002/nep3.70000 · Cited by 9 · see citing works
“43 Boosting the levels of SCFAs with probiotic intervention has been seen to upregulate the neuroprotective phenotype of microglia.”
Radford-Smith, D. E., Oke, K., Costa, C. F. F. A., & Anthony, D. (2025) · Brain, Behavior, & Immunity - Health · doi:10.1016/j.bbih.2025.101013 · Cited by 7 · see citing works
Satheesan, A., Sharma, S., & Basu, A. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01279-3 · Cited by 9 · see citing works
“Butyrate is also reported to have beneficial effects in other major CNS disorders (Bourassa et al. 2016; Cristiano et al. 2022; Guo et al. 2023) Hence, there are mixed evidence regarding the beneficial and detrimental effects of butyrate in viral infections that warrants further investigation.”
BackgroundMai, H. A., Thomas, C. M., Nge, G. G., & Elefant, F. (2025) · Cells · doi:10.3390/cells14120873 · Cited by 9 · see citing works
“NaB was also found to have beneficial effects in brain function and reduced dopaminergic neuron death [112].”
Li, J., Zhao, G., Yu, C., Qu, Y., Shen, X., Zhao, Y., Zhang, J., Lian, W., & Zhao, Y. (2025) · Neuropharmacology · doi:10.1016/j.neuropharm.2025.110596 · Cited by 6 · see citing works
RetractedAdebayo, O. L., Luro, G. E., Akeju, I. D., Onu, C. F., Fawehinmi, M. E., Aderemi, V. A., & Atunnise, A. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01550-9 · Cited by 6 · see citing works
“Butyrate is a short-chain fatty acid produced by colonic bacteria via aerobic fermentation of indigestible dietary fiber (Guo et al. 2023).”
New insights into sodium phenylbutyrate as a pharmacotherapeutic option for neurological disorders
Juárez-Serrano, D., Handal‐Silva, A., Morán-Perales, J. L., Torres-Cifuentes, D. M., Flores, G., Treviño, S., Moreno-Rodriguez, A., Guevara, J., & Díaz, A. (2024) · Synapse · doi:10.1002/syn.22301 · Cited by 5 · see citing works
Weng, S., Zheng, J., Lin, Y., Fang, H., & Ko, C. (2025) · Physiology & Behavior · doi:10.1016/j.physbeh.2025.114864 · Cited by 6 · see citing works
Gudi, C. R., Wannemuehler, M. J., & Mansell, T. J. (2025) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2025.115650 · Cited by 5 · see citing works
Unveiling Butyrate as a Parkinson’s Disease Therapy
Abreu, A. E., Empadinhas, N., & Cardoso, S. M. (2025) · Neuroscience Bulletin · doi:10.1007/s12264-025-01498-x · Cited by 7 · see citing works
Zhang, W., Jiao, Y., Wen, H., Bin, X., Xuefei, W., Lan, J., & Liuyin, Z. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1407241 · Cited by 6 · see citing works
“In addition, it has been found that the use of butyrate in animal models of Parkinson’s disease can improve dyskinesia and dopamine deficiency (83), while propionate seems to be negatively correlated with the Unified Parkinson’s Disease Rating Scale III (84).”
MethodSivamaruthi, B. S., Kesika, P., Chaiyasut, C., & Varman, D. R. (2026) · Frontiers in Microbiology · doi:10.3389/fmicb.2026.1760635 · Cited by 6 · see citing works
The role of the gut microbiome in Parkinson’s disease
Metcalfe‐Roach, A., & Finlay, B. B. (2025) · Future Neurology · doi:10.1080/14796708.2025.2494981 · Cited by 6 · see citing works
Wang, Z., Xia, H., Feng, T., Aibibuli, A., Zhang, M., & Yang, X. (2024) · Neurological Sciences · doi:10.1007/s10072-024-07467-y · Cited by 5 · see citing works
Gut dysbiosis impacts estrogen levels in APP/PS1 transgenic female mice
Romero-Flores, I. S., Garcı́a-Mena, J., & Perez‐Cruz, C. (2025) · Gut Microbes · doi:10.1080/19490976.2025.2599525 · Cited by 5 · see citing works
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- Authors
- Guo, T.-T., Zhang, Z., Sun, Y., Zhu, R.-Y., Wang, F.-X., Ma, L.-J., Jiang, L., & Liu, H.-D.
- Affiliations
- Laboratory of Tissue and Cell Biology, Experimental Teaching Center, Chongqing Medical University, Chongqing 400016, China
- Chongqing Medical University (CN)
- Corresponding author
- Liu, Han-Deng
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2023-02-13
- Volume
- 15
- Issue
- 4
- Pages
- 930
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC9960062
- OpenAlex
- W4320491388
- Cited by
- 82
- References
- 73
- Citations by year
- 2026: 22 · 2025: 33 · 2024: 17 · 2023: 10
- FWCI
- 13.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- the Natural Science Foundation of Chongqing, China (cstc2017jcyjAX0113, CY220404, LTMCMTS2021116)
- the Project of Youth Innovative Talents Training Program of Chongqing (cstc2017jcyjAX0113, CY220404, LTMCMTS2021116)
- the Tutorial System of Medical Undergraduate Foundation of Experimental Teaching Center in Chongqing Medical University (cstc2017jcyjAX0113, CY220404, LTMCMTS2021116)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- sodium butyrate, Parkinson's disease, gut microbiota, gut-brain axis, MPTP-induced neurotoxicity, neuroprotection, dopaminergic neuron death, intestinal barrier disruption, inflammatory cytokines, glial activation, dysbiosis, striatum
- MeSH terms
- Gastrointestinal Microbiome, Animals, Disease Models, Animal, Inflammation, Mice, Inbred C57BL, Parkinson Disease, RNA, Ribosomal, 16S, Neuroprotective Agents, Neurodegenerative Diseases, Butyric Acid, Toll-Like Receptor 4, Mice, Dysbiosis
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