Protective effects of dioscin against Parkinson's disease via regulating bile acid metabolism through remodeling gut microbiome/GLP-1 signaling
Open accessAbstract
It is necessary to explore potent therapeutic agents via regulating gut microbiota and metabolism to combat Parkinson's disease (PD). Dioscin, a bioactive steroidal saponin, shows various activities. However, its effects and mechanisms against PD are limited. In this study, dioscin dramatically alleviated neuroinflammation and oxidative stress, and restored the disorders of mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). 16S rDNA sequencing assay demonstrated that dioscin reversed MPTP-induced gut dysbiosis to decrease Firmicutes-to-Bacteroidetes ratio and the abundances of Enterococcus, Streptococcus, Bacteroides and Lactobacillus genera, which further inhibited bile salt hydrolase (BSH) activity and blocked bile acid (BA) deconjugation. Fecal microbiome transplantation test showed that the anti-PD effect of dioscin was gut microbiota-dependent. In addition, non-targeted fecal metabolomics assays revealed many differential metabolites in adjusting steroid biosynthesis and primary bile acid biosynthesis. Moreover, targeted bile acid metabolomics assay indicated that dioscin increased the levels of ursodeoxycholic acid, tauroursodeoxycholic acid, taurodeoxycholic acid and β-muricholic acid in feces and serum. In addition, ursodeoxycholic acid administration markedly improved the protective effects of dioscin against PD in mice. Mechanistic test indicated that dioscin significantly up-regulated the levels of takeda G protein-coupled receptor 5 (TGR5), glucagon-like peptide-1 receptor (GLP-1R), GLP-1, superoxide dismutase (SOD), and down-regulated NADPH oxidases 2 (NOX2) and nuclear factor-kappaB (NF-κB) levels. Our data indicated that dioscin ameliorated PD phenotype by restoring gut dysbiosis and regulating bile acid-mediated oxidative stress and neuroinflammation via targeting GLP-1 signal in MPTP-induced PD mice, suggesting that the compound should be considered as a prebiotic agent to treat PD in the future.
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Dioscin treatment modifies gut microbiota, bile acid metabolism, and intestinal TGR5 activation, leading to enhanced GLP-1 secretion and reduced glial activation and motor deficits in MPTP-treated mice.
“Notably, the modification of gut microbiota, BA metabolism and activation of intestinal TGR5 by dioscin treatment led to enhanced secretion of GLP-1 in both the intestine and brain of MPTP-treated mice. This is coupled with reduced glial activation and amelioration of motor deficits.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [390]
UDCA and TUDCA have neuroprotective effects in counteracting mitochondrial dysfunction, oxidative stress, and neuroinflammation in Parkinson's disease mouse models.
“Multiple in vivo studies have demonstrated the neuroprotective effects of UDCA and TUDCA in counteracting mitochondrial dysfunction, oxidative stress, and neuroinflammation within PD mouse models.386–392”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [390]
Dioscin treatment activates intestinal TGR5 to stimulate GLP-1 secretion and upregulate GLP-1R expression in the brain, thereby attenuating glial activation and neurodegeneration in MPTP-induced mice.
“The alleviation of MPTP-induced gut dysbiosis and BAs alterations by dioscin treatment activates the intestinal TGR5 to stimulate GLP-1 secretion and upregulate GLP-1R expression in the brain, thereby attenuating glial activation and neurodegeneration.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [390]
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References 76 · Cited by 50
Research works printed but not linked: 1
- [43]Kapoor S. Fitzpatrick M. Clay E. Metabolomics in the Analysis of Inflammatory Diseases Roessner U. Metabolomics 2012 InTech Rijeka (HR) 28045482
- Authors
- Mao, Z., Hui, H., Zhao, X., Xu, L., Qi, Y., Yin, L., Qu, L., Han, L., & Peng, J.
- Affiliations
- Dalian Medical University (CN)
- Yunnan Botanee Biotechnology Group Co. (CN)
- Anhui University of Traditional Chinese Medicine (CN)
- Weifang Medical University (CN)
- Corresponding author
- Qu, Liping
- Han, Lan
- Peng, Jinyong
- Venue
- Journal of Pharmaceutical Analysis
- Publisher
- Elsevier BV
- Published
- 2023-10
- Volume
- 13
- Issue
- 10
- Pages
- 1153-1167
- ISSN
- 2095-1779 (ISSN-L)
- PMC
- PMC10657977
- OpenAlex
- W4380990814
- Cited by
- 50
- References
- 76
- Citations by year
- 2026: 17 · 2025: 20 · 2024: 13
- FWCI
- 8.51
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Pharmaceutical Analysis (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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 › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- dioscin, Parkinson's disease, bile acid metabolism, gut microbiota, GLP-1 signaling, TGR5, bile salt hydrolase, ursodeoxycholic acid, neuroinflammation, oxidative stress, MPTP-induced neurotoxicity, gut dysbiosis, prebiotics, steroidal saponins
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