【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 andincrease 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.