The underlying mechanism of Erbai decoction on Parkinson's disease rats: a behavioral and pathological study.

Abstract

OBJECTIVE: Parkinson's disease (PD) is a highly prevalent degenerative disease of the nervous system, with symptoms of motor retardation and balance disorders. This study aimed to investigate the Erbai decoction on PD rats and explore the underlying mechanism. METHODS: SD rats were divided into five groups, including control, PD, PD + L-Erbai decoction, PD + H-Erbai decoction, and PD + Madopar. Drug treatment was employed with PD rats for 30 days. Firstly, behavioral experiments including the open field test (OFT), pole climbing, tail suspension test (TST), and Morris Water Maze (MWM) were performed. Next, the substantia nigra pars compacta (SNpc) of rats was obtained for H&E and Immunofluorescence (IF) staining, Tunnel, Transmission electron microscopy (TEM), Enzyme-linked immunosorbent assay (ELISA), Flow cytometry, Real-time fluorescence quantitative PCR (RT-qPCR), and Western blotting (WB) assays. Finally, the components of Erbai serum were determined by HPLC-QTOF/MS/MS assay. RESULTS: For the behavioral experiments, it was found that Erbai decoction could enhance the balance and recognition abilities of PD rats. The results of HE and Tunnel revealed that Erbai decoction reversed the rotenone-induced pathological injury of SNpc. In addition, compared with the PD group, the PD + H-Erbai decoction group showed a higher level of autophagy and an inhibition of mitochondrial damage. Moreover, Erbai decoction treatment reversed PD modeling-induced p38 MAPK up-regulation and Parkin down-regulation, and the decrease of Parkin recruitment in mitochondria. Importantly, Erbai decoction and Madopar have similar pharmacological effects. 320 unique components of Erbai serum were identified. CONCLUSION: Erbai decoction could alleviate the SNpc injury by activating mitophagy in PD rats, and it may relate to the regulation of the p38 MAPK/Parkin signaling pathway.