Baicalin alleviates 6-hydroxydopamine-induced neurotoxicity in PC12 cells by down-regulation of microRNA-192-5p.

Parkinson's disease (PD), which is caused by neurodegenerative disorder, has no effective treatment until now. Baicalin was reported to have neuroprotective effects. Hence, we investigated the effects of baicalin on PD in an in vitro cell model by using 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rat pheochromocytoma PC12 cells. PC12 cells were stimulated by 6-OHDA and were treated with baicalin and/or transfected with miR-192-5p mimic or negative control (NC). Cell viability and apoptosis were examined by Cell Counting Kit-8 assay and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) analysis, respectively. The expression of p62, ratio of light chain (LC)3-II/LC3-I, miR-192-5p was detected by qRT-PCR. All protein expression levels were analyzed by western blot. We found that 6-OHDA significantly inhibited cell viability, induced apoptosis and autophagy, while baicalin reversed the results led by 6-OHDA. Moreover, baicalin negatively regulated expression of miR-192-5p. Under baicalin treatment, transfection with miR-192-5p mimic decreased cell viability and induced apoptosis and autophagy in 6-OHDA-treated cells compared with NC. In addition, the phosphorylation of phosphatidylinositol 3'-kinase (PI3K) and protein kinase B (AKT) was statistically down-regulated by baicalin then thereafter reversed by miR-192-5p mimic. Baicalin reduced 6-OHDA-induced cell injury through down-regulation of miR-192-5p, as well as regulation of PI3K/AKT and MDM-2/p53 signal pathways.