Investigating efficacy mechanism of electroacupuncture in treating Parkinson disease through TMT proteomics

To explore the therapeutic mechanism of electroacupuncture (EA) in treating Parkinson disease (PD) using Tandem mass tag (TMT) quantitative proteomics technology.

Forty-eight PD patients were randomly divided into a control group and an observation group, with 24 patients in each group. The control group received routine drug treatment, while the observation group received EA in addition to the routine drug treatment. EA was administered for 30 min per session, 3 times a week, for a total of 12 weeks. Nine patients from each group were randomly selected to provide peripheral blood serum samples before and after treatment for TMT quantitative proteomics analysis. Differentially expressed proteins between the two groups were compared, and bioinformatics analysis was performed. The screened differentially expressed proteins were validated using enzyme-linked immunosorbent assay (ELISA).

In the observation group, scores on the unified Parkinson disease rating scale (UPDRS), UPDRS II, and UPDRS III were significantly reduced after treatment (P<0.05). In the control group, these scores tended to increase, but the changes were not statistically significant (P>0.05). After treatment, the UPDRS and UPDRS III scores in the observation group were significantly lower than those in the control group (P<0.05). The observation group showed 62 differentially expressed proteins, while the control group had 36. Compared to the control group, the observation group had 142 differentially expressed proteins. These proteins were primarily involved in the cyclic adenosine monophosphate (cAMP) signaling pathway, T helper (Th) 1 and Th2 cell differentiation, ATP-binding cassette transporter, vascular endothelial growth factor signaling pathway, and high-affinity immunoglobulin E receptor (FcεRI) signaling pathway. ELISA verification indicated that after EA treatment, the levels of α-Synuclein (αSyn) and heat shock protein beta 1 (HSPB1) in the observation group were significantly lower than those in the control group (P<0.05), while the regulator of G-protein signaling 10 (RGS10) level was significantly higher (P<0.05).

EA, combined with routine drug therapy, can significantly improve clinical symptoms of PD, potentially through the regulation of the cAMP signaling pathway and the contents of differentially expressed proteins of αSyn, HSPB1, and RGS10.