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Sodium butyrate ameliorates the impairment of synaptic plasticity by inhibiting the neuroinflammation in 5XFAD mice
Abstract
Current strategies for the treatment of Alzheimer's disease (AD) focus on the pathology in the later stages of disease progression. Early microglia abnormality and β-amyloid (Aβ) deposition trigger disease development before identical symptoms emerge, which leads to poor clinical treatment effects in the later stages. In the early stage of disease progression, microglia in brains of 5XFAD mice have been activated by Aβ plaques to secrete more pro-inflammatory cytokines. In the meantime, these cytokines up-regulate Aβ via increasing the APP processing. Sodium butyrate (NaB), as one of the short chain fatty acid (SCFA) generated by gut microbiota, is the inhibitor of histone deacetylase (HDAC), which reduces the secretion of pro-inflammatory cytokines. In our experiment, 8-week-old 5XFAD mice and their litter WT mice were treated with NaB or normal saline for 2 weeks (WT + Vehicle group, WT + NaB group, AD + Vehicle group and AD + NaB group). After treatment, behavioral tests were carried out. The novel object recognition (NOR) and Morris water maze (MWM) tests demonstrated that there was no significant difference between four groups of mice. The results of long-term potentiation (LTP) and depotentiation (DEP) illustrated that the synaptic plasticity was promoted in 5XFAD mice after treatment with NaB. Compared to the AD + Vehicle group, the dendritic spines were more abundant in other groups of mice. Furthermore, the synapse-associated proteins (PSD-95, SYP, NR2B) were reduced and the pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) were increased in the AD + Vehicle group. These phenomena were reversed after treatment with NaB. Moreover, our results suggested that NaB suppressed the over-activation of microglia and the accumulation of Aβ in AD mice. Altogether, all results illustrated that HDAC inhibitor NaB could ameliorate the synaptic plasticity by reducing neuroinflammation in 5XFAD mice in the early stage of the disease.
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“Studies have demonstrated the neuroprotective effects of sodium butyrate in 5xFAD mice by inhibiting microglial activation and promoting synaptic plasticity (Fig. 3a).299,300”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [300]
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Metadata
- Authors
- Jiang, Y., Li, K., Li, X., Xu, L., & Yang, Z.
- Affiliations
- Nankai University (CN)
- Corresponding author
- Yang, Zhuo
- Venue
- Chemico-Biological Interactions
- Publisher
- Elsevier BV
- Published
- 2021-05
- Volume
- 341
- Pages
- 109452
- ISSN
- 0009-2797 (ISSN-L)
- OpenAlex
- W3146836254
- Cited by
- 154
- References
- 54
- Citations by year
- 2026: 24 · 2025: 33 · 2024: 29 · 2023: 39 · 2022: 23 · 2021: 6
- FWCI
- 15.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Chemico-Biological Interactions (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- sodium butyrate, Alzheimer's disease, synaptic plasticity, neuroinflammation, microglial activation, amyloid-beta, 5xFAD mice, histone deacetylase inhibition, short-chain fatty acids, inflammatory cytokines, long-term potentiation, dendritic spines, synaptic proteins, early Alzheimer's disease
- MeSH terms
- Disks Large Homolog 4 Protein, Morris Water Maze Test, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Inflammation, Mice, Transgenic, Neuronal Plasticity, Amyloid beta-Peptides, Synaptophysin, Microglia, Long-Term Potentiation, Butyric Acid, Cognitive Dysfunction
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