Objective：To explore the effects of cell injury and the expression of inflammation related genes in rat microglial cells induced by methamphetamine(Meth). Methods：Cell viability and apoptosis induced by Meth were detected by MTT and in situ end labeling(TUNEL) after primary culture of SD fetal rat microglial cells.The effect of Meth on the expression of inflammatory cytokines mRNA in the microglial cells was evaluated by real time fluorescence quantitative polymerase chain reaction(real-time PCR).The secretion of interleukin(IL)-6，tumor necrosis factor(TNF)-α and inducible nitric oxide synthase(iNOS)in microglia cells induced by Meth were detected by ELISA method. Results：MTT showed that Meth reduced microglia viability in a concentration dependent manner(25，50，100，and 200 μmol/L) with statistically significant at a concentration of 200 μmol/L(P＜0.05). TUNEL results showed that 200 μmol/L Meth significantly contributed to cell apoptosis compared with the control group(P＜0.05). Q-PCR results showed that Meth reduced the expression levels of IL-24 and nitric oxide synthase 3(NOS3) in microglial cells for 24 hours. However，the expression levels of Peli3，Sigma receptor 1(sig1)-R，IL-1，IL-6 and Toll like receptor 4(TLR4) were up-regulated. In addition，protein levels were also confirmed that Meth promoted the secretion of IL-6 and TNF-α. Conclusion：Meth exposure obviously contributes to microglial damage. Moreover，it causes IL-1β，IL-1R，IL-6，TLR4 and other inflammatory factors mRNA expression changes，and promotes the secretion of IL-6 and TNF-α，which may damage the central nervous system，resulting in neurotoxicity.