# Electroacupuncture exerts neuroprotective effects and alters gut microbiota in a MPTP-induced mouse model of Parkinson’s disease

**Authors:** Xi-Chen Wu, Yi-Yue Dong, Yu-Chen Ying, Guang-Yan Chen, Xi Wang, Qian Fan, Ping Yin, Yue-Lai Chen

PMC · DOI: 10.3389/fnins.2025.1702912 · Frontiers in Neuroscience · 2026-01-14

## TL;DR

Electroacupuncture helps protect brain function and improves gut health in a mouse model of Parkinson’s disease.

## Contribution

This study reveals that electroacupuncture can alter gut microbiota and protect dopaminergic neurons in Parkinson’s disease.

## Key findings

- EA improved motor deficits and restored tyrosine hydroxylase expression in the brain.
- EA enhanced gut barrier integrity and normalized the abundance of specific gut microbes.
- EA simplified microbial interactions and improved network stability in the gut.

## Abstract

To investigate the therapeutic mechanism of electroacupuncture (EA) in a mouse model of Parkinson’s disease (PD) induced by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

Motor functions were evaluated using open field test and pole tests. Tyrosine hydroxylase (TH) expression in the substantia nigra and striatum was detected by immunohistochemistry. Intestinal barrier integrity was assessed via immunofluorescence staining of tight junction proteins ZO-1 and Occludin. Gut microbiota composition was analyzed by 16S rRNA sequencing.

EA treatment significantly improved motor deficits, restored TH expression in nigrostriatal regions, and enhanced colonic ZO-1 and Occludin levels. EA reversed MPTP-induced dysbiosis, notably normalizing the abundances of Dubosiella, Lactobacillus, Enterococcus, Desulfovibrio, Bacteroides, Allobaculum, and Parasutterella. Microbial co-occurrence network analysis revealed that EA simplified hyperconnected interactions and improved network stability.

EA treatment attenuated PD progression, which was associated with the remodeling of gut microbiota structure and restoration of microbial network stability. The concomitant protection of dopaminergic function suggests a potential link mediated by the gut–brain axis.

## Linked entities

- **Proteins:** TJP1 (tight junction protein 1), si:ch73-61d6.3 (uncharacterized si:ch73-61d6.3)
- **Chemicals:** 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (PubChem CID 1388)
- **Diseases:** Parkinson’s disease (MONDO:0005180)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Ocln (occludin) [NCBI Gene 18260] {aka Ocl}, Th (tyrosine hydroxylase) [NCBI Gene 21823], Tjp1 (tight junction protein 1) [NCBI Gene 21872] {aka ZO1}
- **Diseases:** motor deficits (MESH:D009461), PD (MESH:D010300)
- **Chemicals:** 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MESH:D015632)
- **Species:** Allobaculum (genus) [taxon 174708], Mus musculus (house mouse, species) [taxon 10090], Enterococcus (genus) [taxon 1350], Desulfovibrio (genus) [taxon 872], Lactobacillus (genus) [taxon 1578], Bacteroides (genus) [taxon 816], Parasutterella (genus) [taxon 577310]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12847003/full.md

## References

95 references — full list in the complete paper: https://tomesphere.com/paper/PMC12847003/full.md

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Source: https://tomesphere.com/paper/PMC12847003