Rifampicin protects rotenone-induced mitochondrial damage in differentiated PC12 cells

Objective To explore the effects ofrifampicin(RFP)on the cell viability.reactive oxygen species(ROS)formation,the change of mitochondrial transmembrance potential(△ψm)and cell apoptosis induced by rotenone(Rot)in differentiated PC12 cells.Methods Rot was added to make a model ofParkinson's disease in rat pheochromocytoma(PCI2)cells in the presence of RFP.Cell viability was determined by MTT assay.Change of △ψm and cell apoptosis were measured by fluorescence microscope and flow cytometry respectively.Results Compared with control group and 300 μmol/L RFP group,cell viability was significantly decreased but depolarization of △ψm,ROS formation and cell apoptosis rate were significantly increased in 2.5 μmol/L Rot group.Compared with 2.5 μmol/L Rot group,RFP(100,200 and 300 μmol/L)pretreated groups,cell viability was significantly increased,but depolarization of △ψm、ROS formation and cell apoptosis rate were significantly decreased in a dose-dependent manner.Conclusion RFP may protect the damage induced by Rot in differentiated PC12 by reducing depolarization of △ψm and ROS formation in a dose-dependent manner. Key words: Rifampicin; Rotenone; Reactive oxygen species; Mitochondrial transmembrance potential; Parkinson's disease