Electroacupuncture suppresses motor impairments via microbiota-metabolized LPS/NLRP3 signaling in 6-OHDA induced Parkinson's disease rats

Aug 21, 2025International immunopharmacology

Electroacupuncture reduces movement problems by affecting gut bacteria-related inflammation in a rat model of Parkinson's disease

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Abstract

Electroacupuncture (EA) significantly improved motor and anxiety symptoms in a 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease.

EA treatment elevated levels of tyrosine hydroxylase (TH), a key enzyme in dopamine synthesis.
Metabolomic analysis indicated that the therapeutic effects of EA are linked to changes in the gut microbiota and the NOD-like receptor signaling pathway.
EA altered the composition of the gut microbiota, affecting the relative abundance of 16 genera.
The treatment led to downregulation of the lipopolysaccharide (LPS) and NOD-like receptor signaling pathways.
EA reduced intestinal inflammation and decreased serum inflammatory markers, which may contribute to its protective effects.
Fecal microbiota transplantation experiments suggested that gut microbiota plays a crucial role in mediating the anti-Parkinson's disease effects of EA.

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Emerging evidence indicates that electroacupuncture (EA) exerts significant therapeutic effects on Parkinson's disease (PD)-related symptoms, with the immune mechanisms of the gut-brain axis playing a pivotal role in PD pathophysiology. This study aimed to explore whether EA mitigated PD-related symptoms and conferred neuroprotection to dopaminergic neurons in a 6-hydroxydopamine (6-OHDA) rat model by modulating the microbiota-metabolized lipopolysaccharide (LPS)/NLRP3 pathway. EA treatment ameliorated motor and anxiety symptoms in 6-OHDA rats and elevated the levels of TH. Metabolomic analysis indicated that the therapeutic effects of EA are associated with the gut microbiota and the NOD-like receptor signaling pathway. 16S rRNA sequencing demonstrated that EA significantly modified the composition of the gut microbiota, evidenced by alterations in the relative abundance of 16 genera, and led to the downregulation of the LPS and NOD-like receptor signaling pathways. Additionally, EA was found to attenuate intestinal inflammation, decrease serum inflammatory markers, reduce neuroinflammation, and suppress the overexpression of microglia and astrocytes, while concurrently preserving the integrity of the intestinal and blood-brain barriers. Fecal microbiota transplantation experiments further substantiated the pivotal role of gut microbiota in mediating the anti-PD effects of EA. In summary, EA has the potential to alleviate PD-related symptoms and safeguard dopaminergic neurons by rectifying gut microbiota dysbiosis and downregulating the LPS/NLRP3 immune pathway along the gut-brain axis in PD rat models.

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