OBJECTIVE: To study the toxicity and its mechanisms of 1-methyl-4-phenylpyridinium ion (MPP+) on pheochromocytoma PC12 cells.METHODS: PC12 cells were cultured in vitro, and poisoned by 100, 300, 500 micromol/L MPP+. Western blot was performed to determine the level of phosphorylated c-Jun-N-terminal kinase/stress activated protein kinases (JNK/SAPK). The cells were pretreated with SP600125, an inhibitor of JNK pathway, and then the number of apoptotic cells were counted by using TUNEL stain, observing its influence on cell apoptosis seduced by MPP+.RESULTS: MPP+ poisoning can cause the increase of phosphorylation level of JNK1/2 cells. The usage of JNK pathway inhibitor SP600125 can inhibit the PC12 cell apoptosis seduced by MPP+.CONCLUSION: Activation of JNK pathway may be the important molecular mechanism of PC12 cell apoptosis seduced by MPP+ and of producing dopaminergic neurotoxicity.
1-Methyl-4-phenylpyridinium Animals