Evidence map›Paper›PMID 41761283›Full record

ArticleTranslational neurodegeneration2026

Bacteroides coprocola protects dopaminergic neurons in rotenone-induced Parkinson's disease mouse model by modulating gut microbiota dysbiosis and inhibiting the NLRP3 signaling pathway.

Zixian Liu, Jiabei Nie, Yimei Li, Maoxin Huang, Ziluo Chen, Shushang Yu, Jiaqi Zheng, Yuyan Tan, Shengdi Chen

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PubMed Full text at PMC Publisher
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Article in Translational neurodegeneration, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Zixian LiuLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China.ORCID http://orcid.org/0009-0005-1998-1093
Jiabei NieDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Yimei LiLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China.
Maoxin HuangDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Ziluo ChenLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China.
Shushang YuLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China.
Jiaqi ZhengLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China.
Yuyan TanDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. tyy11672@rjh.com.cn.ORCID http://orcid.org/0000-0003-1779-6554
Shengdi ChenLab for Translational Research of Neurodegenerative Diseases, Shanghai Institute for Advanced Immunochemical Studies (SIAIS) and School of Life Science and Technology, Shanghai Tech University, Shanghai, 201210, China. chensd@rjh.com.cn.ORCID http://orcid.org/0000-0002-6242-1025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is a prevalent neurodegenerative disease and its pathogenesis is still unclear. Emerging evidence supports the gut-origin hypothesis, highlighting gut microbiota dysbiosis as a contributing factor in PD pathogenesis. Our previous clinical study showed that Bacteroides coprocola (B. coprocola), a gut bacterium producing short-chain fatty acids (SCFAs), was significantly reduced in PD patients. This study was aimed to investigate the potential of B. coprocola in ameliorating PD pathology and explore the underlying mechanisms in a rotenone-induced PD mouse model.

methodsThe rotenone-induced PD mouse model was treated by orally administering B. coprocola for three weeks. Immunofluorescence, Western blotting, flow cytometry, 16S rRNA sequencing, and metabolomics were performed to assess midbrain and intestinal changes, NLRP3 inflammasome activation, macrophage polarization, gut microbiota, and SCFA levels. In vitro, LPS-stimulated bone marrow-derived macrophages were used to validate the role of NLRP3 signaling in macrophage polarization following sodium acetate and sodium butyrate treatment via siRNA and molecular assays.

resultsB. coprocola treatment alleviated PD-related motor deficits, neuroinflammation, gut microbiota dysbiosis, and intestinal barrier permeability in the rotenone-induced PD mouse model. Mechanistically, B. coprocola reshaped the gut microbiota composition and modulated macrophage polarization, which were associated with the inhibition of the NLRP3 inflammasome signaling pathway. Furthermore, in vitro experiments confirmed that the acetate and butyrate-key metabolites of B. coprocola-attenuated the inflammatory responses and promoted M2-like macrophage polarization via free fatty acid receptor (FFAR) 2/3 receptors, thereby suppressing NLRP3 activation.

conclusionsIn conclusion, B. coprocola treatment can improve motor deficits, neuroinflammation, and intestinal function in the rotenone-induced PD mouse model. The effects are associated with microbiota remodeling, regulation of macrophage polarization, and inhibition of the NLRP3 inflammasome pathway. Acetate and butyrate, key metabolites of B. coprocola, might play an important role in promoting M2 macrophage polarization through FFAR2/3 receptors.

Indexed as

BacteroidesDopaminergic NeuronsDysbiosisGastrointestinal MicrobiomeNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLParkinson DiseaseRotenoneSignal TransductionNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseRotenoneAcetateButyrateFFAR2FFAR3Gut microbiotaMacrophage polarizationNLRP3 signaling pathwayParkinson’s disease

Identifiers

PMID41761283
PMCPMC12949511

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.