Minocycline inhibits MPP~+-induced apoptosis and mitochondrial dysfunction in PC12 cells

AIM: To explore the effect of minocycline on 1-methyl-4-phenylpyridinium ion(MPP+)-induced apoptosis and mitochondrial dysfunction in PC12 cells.METHODS: PC12 cells were used as an apoptotic model of dopaminergic neurons,and minocycline or MPP+ was added into the culture system.MTT assay was used to observe the cell viability.DCFH-DA was used as the probe to detect the level of reactive oxygen species(ROS),and JC-1 probe was employed to measure mitochondrial menbrane potential in PC12 cells.RESULTS: The viability of PC12 cells decreased by 80.8% after 24 h exposure to 0.5 mmol/L MPP+.Meanwhile,the concentration of ROS was increased to 230.0% and mitochondrial depolarization in PC12 cells was detected.Minocycline at 10 μmol/L significantly blocked the effects of MPP+,such as decreasing cell viability,inducing cell apoptosis and decreasing mitochondrial membrane potential.CONCLUSION: Minocycline protects mitochondria from dysfunction induced by MPP+ in PC12 cells.