Short-Chain Fatty Acid Aggregates Alpha-Synuclein Accumulation and Neuroinflammation via GPR43-NLRP3 Signaling Pathway in a Model Parkinson’s Disease
Abstract
Parkinson's disease (PD) is characterized by the aggregation of α-synuclein (α-syn) and the loss of dopaminergic (DA) neurons, with growing evidence suggesting a significant role of gut microbiota and their metabolites in the disease's pathogenesis. This study explores the effects of short-chain fatty acids (SCFAs) on PD progression, focusing on the G protein-coupled receptor 43 (GPR43) and the NLRP3 signaling pathway in both in vitro and in vivo models. Employing the1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model and SH-SY5Y cells with SCFAs-treated, this study investigated the impact of SCFAs on α-syn deposition, DA loss, and neuroinflammation. In vitro, supernatant from STC-1 cells was administered to SH-SY5Y cells, and the effects were assessed following the knockdown of NLRP3 or GPR43. In vivo, mice were treated with NLRP3 or GPR43 inhibitors after feeding with SCFAs, and the motor deficits, α-syn pathology, DA neuronal loss, and inflammatory responses were observed. SCFAs were found to exacerbate motor and gastrointestinal dysfunctions in PD models, intensifying α-syn pathology and neuroinflammation. The activation of the NLRP3 inflammasome through GPR43 emerged as a key pathological mechanism, with inhibition of these molecules mitigating the observed effects. Such interventions reduced α-syn accumulation, DA loss, and inflammatory responses, highlighting the pivotal role of the SCFA/GPR43-NLRP3 pathway in PD. The findings from this study elucidate a critical link between gut-derived metabolic changes and neuroinflammatory processes in PD via the SCFA/GPR43-NLRP3 pathway. Targeting this pathway offers a promising therapeutic strategy and enriches our understanding of the gut-brain axis' role in PD progression.
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In vitro data indicate that SCFAs might contribute to α-synuclein pathogenesis.
“At the molecular level, in vitro data indicate that SCFAs might contribute to α-synuclein pathogenesis.”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [123]
SCFAs are shown to modulate activation of the NLRP3 inflammasome via GPR43 activation and modulation of autophagy pathways via autophagy genes including Atg5 and the PI3K/Akt/mTOR pathway.
“SCFAs are shown to modulate activation of the NLRP3 inflammasome via GPR43 activation and modulation of autophagy pathways via autophagy genes including Atg5 and the PI3K/Akt/mTOR pathway. [123, 124].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [123]
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Hou, X., Li, Y., Mu, W., Wang, H., & Ji, S. (2026) · Frontiers in Nutrition · doi:10.3389/fnut.2026.1941474
Roles of growth factor-mediated brain-gut axis crosstalk in neurorepair following ischemic stroke
Li, M., Bo, W. A. N. G., & Ma, Y. (2026) · Journal of Zhejiang University (Medical Sciences) · doi:10.3724/zdxbyxb-2026-0250
- Authors
- Qu, Y., An, K., Wang, D., Yu, H., Li, J., Min, Z., Xiong, Y., Xue, Z., & Mao, Z.
- Affiliations
- Tongji Hospital (CN)
- Corresponding author
- Mao, Zhijuan
- Venue
- Molecular Neurobiology
- Published
- 2025-02-04
- Volume
- 62
- Issue
- 5
- Pages
- 6612-6625
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W4407126718
- Cited by
- 30
- References
- 57
- Citations by year
- 2026: 15 · 2025: 15
- FWCI
- 18.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81901303)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, short-chain fatty acids, alpha-synuclein aggregation, GPR43, NLRP3 inflammasome, neuroinflammation, dopaminergic neuron loss, gut microbiota metabolites, gut-brain axis, MPTP mouse model, SH-SY5Y cells, STC-1 cells, motor impairment, gastrointestinal dysfunction
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Neuroinflammatory Diseases, Animals, Disease Models, Animal, Fatty Acids, Volatile, Humans, Male, Mice, Inbred C57BL, Parkinson Disease, Signal Transduction, Receptors, G-Protein-Coupled, Cell Line, Tumor, Mice, alpha-Synuclein, Dopaminergic Neurons, Protein Aggregates
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