Toxicol Lett 2012,
Li, Yan; Hu, Zhengtao; Chen, Bo; Bu, Qian; Lu, Wenjie; Deng, Yi; Zhu, Ruiming; Shao, Xue; Hou, Jing; Zhao, Jinxuan; Li, Hongyu; Zhang, Baolai; Huang, Yina; Lv, Lei; Zhao, Yinglan; Cen, Xiaobo
Methamphetamine (METH), a commonly abused psychostimulant, has been shown to induce neuronal damage by causing reactive oxygen species (ROS) formation, apoptosis and autophagy. Taurine (2-aminoethanesulfonic acid) is involved in several physiological actions in the brain, including neuroprotection, osmoregulation and neurotransmission. In this study, we investigate the protective effect of taurine against METH-induced neurotoxicity in PC12 cells and the underlying mechanism. The results showed that taurine significantly increased the cell viability inhibited by METH. LC3-II expression was elevated by METH treatment, whereas such increase was obviously attenuated by taurine. Co-treatment of taurine strongly reversed the decline of antioxidase activities induced by METH. Moreover, phosphorylated mammalian target of rapamycin (p-mTOR) was significantly inhibited by METH, whereas complementation of taurine markedly increased the expression of p-mTOR in PC12 cells, rather than phosphorylated Erk. Interestingly, taurine-induced decreasing expression of LC3-II was partially blocked by pretreatment of RAD001, an mTOR inhibitor. These results indicated that taurine inhibits METH-induced autophagic process through activating mTOR rather than Erk signaling. Collectively, our study shows that taurine protects METH-induced PC12 cells damage by attenuating ROS production, apoptosis and autophagy, at least in part, via mTOR signaling pathway.
Diseases/Pathways annotated by Medline MESH:
MAP Kinase Signaling System
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mTOR ⊣ RAD001: " Interestingly, taurine induced decreasing expression of LC3-II was partially blocked by pretreatment of RAD001
, an mTOR
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