JNK通路在MPP^+诱导PC12细胞凋亡中的作用

Effect of JNK pathway in apoptosis of PC12 cell by MPP^+

目的研究1-甲基-4-苯基-吡啶离子(MPP+)对PC12细胞的毒性作用及其机制。方法 PC12细胞体外培养,以100、300、500μmol/L MPP+进行染毒。Western blot法检测JNK1/2磷酸化水平;使用JNK通路阻断剂SP60012预处理细胞,TUNEL法观察其对MPP+诱导的细胞凋亡的影响。结果 MPP+染毒可以引起细胞JNK1/2的磷酸化水平增高,使用JNK通路阻断剂SP600125可以抑制MPP+诱导的PC12细胞凋亡。结论激活JNK通路可能是MPP+诱导PC12细胞凋亡、产生多巴胺能神经毒性的重要分子机制。

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 μmol/L MPP＋.Western blot was performed to determine the level of phosphorylated c-Jun-N-terminal kinase/ stressactivated 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 apotosis seduced by MPP^＋.Results MPP^＋ poisoning can cause the increase of phosphorlation level of JNK1 /2 cells.The usage of JNK pathway inhibitor SP600125 can inhibit the PC12 cell apotosis seduced by MPP^＋.Conclusion Activation of JNK pathway may be the important molecular mechanism of PC12 cell apotosis seduced by MPP^＋ and of producing dopaminergic neurotoxicity.