The effect of electroacupuncture at ST25 on Parkinson's disease constipation through regulation of autophagy in the enteric nervous system.

The effectiveness and safety of electroacupuncture (EA) for constipation have been confirmed by numerous clinical studies and experiments, and there are also studies on the efficacy of EA for Parkinson's disease (PD) motor symptoms. However, there are few researches on EA for PD constipation. Autophagy is thought to be involved in the mechanistic process of EA in the central nervous system (CNS) intervention in Parkinson's pathology. However, whether it has the same effect on the enteric nervous system (ENS) has not been elucidated. Therefore, we investigated whether EA at Tianshu (ST25) acupoint promotes the clearance of α-Syn and damaged mitochondria aggregated in the ENS in a model of rotenone-induced PD constipation. This study evaluated constipation symptoms by stool characteristics, excretion volume, and water content, and the expression levels of colonic ATG5, LC3II, and Parkin were detected by Western Blot (WB) and Real-Time Quantitative PCR (RT-qPCR). The relationship between the location of α-Syn and Parkin in the colonic ENS was observed by immunofluorescence (IF). The results showed that EA intervention significantly relieved the symptoms of rotenone-induced constipation in PD rats, reversed the rotenone-induced down-regulation of colonic ATG5, LC3II, and Parkin expression, and the positional relationship between colonic α-Syn and Parkin proved to be highly correlated. It is suggested that EA might be helpful in treating PD constipation by modulating Parkin-induced mitochondrial autophagy.

Parkinson's disease constipation effect of electroacupuncture at ST25 through colonic motility and enteric neuropathology.

Background: The enteric nervous system (ENS) plays a central role in developing Parkinson's disease (PD) constipation, and the regulation of the ENS may be a key component in treating PD constipation. Electroacupuncture (EA) can effectively treat constipation symptoms in PD, but research on its specific mechanisms, especially in terms of ENS, is relatively lacking. Therefore, we investigated whether EA at ST25 promotes the restoration of ENS structure and colonic motor function in the rotenone-induced PD constipation rat model. Methods: In this study, we evaluated constipation symptoms by stool characteristics, excretion and water volume, and whole gut transit time and observed colonic motility regulation through colonic motion detection and pathological changes in the colonic myenteric nervous plexus by transmission electron microscopy and immunofluorescence staining. Results: EA significantly improved the constipation symptoms and positively adjusted the colonic motility in rotenone-induced PD constipation rats. At the same time, EA reversed the rotenone-induced colonic myenteric nervous plexus injury and regulated the ratio of inhibitory and excitatory neurotransmitters. Conclusion: Our results indicate that EA treatment of PD constipation may be mediated through the adjustment of ENS.