Propofol protects PC12 cells from cobalt chloride-induced injury by mediating miR-134

Objective. Propofol (PRO) was reported to exert a neuroprotective effect by decreasing microRNA-134 (miR-134), a brain-specific miRNA, thus, the role of PRO against cobalt chloride (CoCl2)-induced injury in rat pheochromocytoma cells (PC12) via mediating miR-134 was explored. Methods. CoCl2-induced PC12 cells treated with PRO were transfected with or without miR-134 negative control (NC)/ inhibitor/ mimic, and the following detections were then performed using cell counting kit-8 (CCK-8), Annexin V-fluorescein isothiocyanate/propidium iodide (Annexin V-FITC/ PI) and Hoechst 33258 staining. Autophagy was observed by transmission electron microscope (TEM). Mitochondrial membrane potential (MMP) was detected by Rhodamine-123 (Rh123) staining, and reactive oxygen species (ROS) by dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining. Protein and gene expressions were measured by Western blotting and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), respectively. Results. PRO reversed the CoCl2-induced decrease in the PC12 cell viability and increased miR-134 in a dose- dependent manner. CoCl2 increased LC3II/I ratio and Beclin-1 expression, but decreased p62 expression, which was abolished by PRO. In addition, an increased cell apoptosis rates triggered by CoCl2 were reduced by PRO with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2. Furthermore, PRO decreased methylenedioxyamphetamine (MDA), nitric oxide (NO) and ROS in CoCl2- induced PC12 cells accompanying the increase in glutathione peroxidase (GSH-Px) and MMP. The effects of PRO on autophagy, apoptosis and oxidative stress in CoCl2-induced PC12 cell were reversed by miR-134 mimic. Conclusion. PRO may mitigate CoCl2-induced autophagy in PC12 cells with decreased apoptosis and improved oxidative stress via mediating miR-134.

Automated summary

The study reveals that propofol can attenuate cobalt chloride-induced injury in PC12 cells by decreasing apoptosis and improving oxidative stress, potentially through mediating miR-134.