The protective effect of decoction of Rehmanniae via PI3K/Akt/mTOR pathway in MPP+-induced Parkinson's disease model cells.

This research aims to explore the function of DOR in 1-methyl-4-phenylpyridinium (MPP+)-induced Parkinson's disease model cell SH-SY5Y. SH-SY5Y cells were exposed with various doses of MPP + or DOR. Cell counting Kit-8 (CCK-8) assay and flow cytometry (FCM) were used to detect the cell viability, apoptosis and reactive oxygen species (ROS) levels in MPP+ Parkinson's disease model cells SH-SY5Y. The oxidative stress markers were measured by Enzyme-linked immunosorbent assay (ELISA), Western blot and quantitative real-time reverse transcription PCR (qRT-PCR) assays. To further determine the protective effect of DOR on acute injury via PI3K/Akt/mTOR pathway, cells were treated with LY294002 (LY), a PI3K/Akt/mTOR pathway inhibitor, with MMP + or DOR or not. MPP+ at various doses caused cell injury with decrease of viability, increase of apoptosis and ROS level, while DOR partly prevented the cell against injury induced by MPP+. Bax, Cyt-c and cleaved-Caspase-12, 9 and 3 were increased, and meanwhile Bcl-2 was decreased in MPP+ stimulated cells, while those changes could be partly inhibited by DOR incubation. Furthermore, the phosphorylation level of PI3K, AKT and mTOR was suppressed by MPP+, while DOR treatment could enhanced the level of phosphorylated-PI3K (p-PI3K), AKT (P-AKT) and mTOR. LY aggravated the injury of SH-SY5Y cells treated with MPP+, and DOR could partly alleviate those effects. DOR had a protective effect against MPP+ induced injury of Parkinson's disease model cell through activating the PI3K/Akt/mTOR pathway. It suggests that DOR should be further explored in Parkinson's disease.