Regulation of miR-133b on Methamphetamine-induced Neuronal Apoptosis in PC12 Cells / 中山大学学报(医学科学版)

ABSTRACT

[Objective]To investigate the expression changes of miR-133b in methamphetamine(MA)-induced neuro-nal injury in PC12 cells and its regulative effects on cellular apoptosis.[Methods]PC12 cells were cultured and divided into control group and MA treated group.In MA treated group,PC12 cells were insulted with 800μmol/L MA in culture medium. The cellular injury of PC12 cells was observed under microscope. The cellular apoptosis was detected by Hoechst33342/PI double staining,and the expression level of miR-133b was examined by real-time quantitative PCR(RT-PCR). Further-more,miR-133b mimic and inhibitors were transfected into PC12 cells to analyze miR-133b's function in MA-induced cell apoptosis.[Results]The data showed that 800 μmol/L MA could induce obvious cellular injury,cause neurite shortened and increase the cell apoptosis. The RT-PCR data showed that the expression of miR-133b of PC12 cells treated with MA de-creased significantly.The apoptosis rate of PC12 cells decreased after transfection of miR-133b mimic,while increased after transfection of miR-133b inhibitors.[Conclusions]High concentration of MA causes neuron damage and induces neuronal apoptosis,and also decreases the levels of miR-133b expression. Whereas,overexpression of miR-133b can reduce the apoptosis of cultured PC12 cells.Thus,miR-133b plays a crucial role in MA mediated neurotoxicity.This study provides a theoretical basis for elucidating the mechanism of MA-induced neurotoxicity and may provide a new strategy for treating MA addiction.