Rifampicin protects rotenone-induced mitochondrial damage in differentiated PC12 cells
10.3760/cma.j.issn.1671-8925.2009.09.011
- VernacularTitle:利福平对鱼藤酮诱导的分化PC12细胞线粒体损伤的保护作用
- Author:
Shi-Wen CHEN
1
;
Yuan-Lin SUN
;
Zhi-Fen ZENG
;
En-Xiang TAO
Author Information
1. 广东省江门市中心医院
- Keywords:
Rifampicin;
Rotenone;
Reactive oxygen species;
Mitochondrial transmembrance potential;
Parkinson's disease
- From:
Chinese Journal of Neuromedicine
2009;8(9):907-910
- CountryChina
- Language:Chinese
-
Abstract:
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.
