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目的研究1-甲基-4苯基-吡啶离子(MPP+)对大鼠嗜铬细胞瘤PC12细胞增殖的抑制作用及其分子机制。方法PC12细胞体外培养,分别以100,300,500μmol/L MPP+进行染毒。四甲基偶氮噻唑蓝法(MTT)观察MPP+对细胞的抑制作用;免疫印迹法检测细胞ERK1/2表达及磷酸化水平。结果不同剂量以及不同作用时间的MPP+对PC12细胞增殖有明显的抑制作用,抑制率为18.86%~58.06%。MPP+可以抑制细胞外调节信号激酶(ERK)的磷酸化水平,其中300μmol/L MPP+染毒3 d时,ERK磷酸化水平约为对照组的4.7%。ERK通路阻断剂PD98059与300μmol/L MPP+共同作用时,对细胞增殖的抑制率增高至78.9%。结论MPP+可以明显抑制PC12细胞的增殖,降低ERK的磷酸化水平可能是其重要分子机制之一。
Objective To investigate the inhibitory effect of 1-methyl-4-phenyl-pyridinium (MPP +) on the proliferation of PC12 cells in rat pheochromocytoma and its molecular mechanism. Methods PC12 cells were cultured in vitro and exposed to 100, 300 and 500 μmol / L MPP +, respectively. The inhibitory effect of MPP + on cells was observed by MTT assay. The expression of ERK1 / 2 and the phosphorylation of ERK1 / 2 were detected by Western blotting. Results MPP + at different doses and different time significantly inhibited the proliferation of PC12 cells with the inhibitory rates of 18.86% -58.06%. MPP + could inhibit the phosphorylation of extracellular regulated signal kinase (ERK), and the phosphorylation level of ERK was about 4.7% of the control group after 300μmol / L MPP + 3 days. ERK pathway inhibitor PD98059 combined with 300μmol / L MPP +, the inhibition of cell proliferation increased to 78.9%. Conclusion MPP + can significantly inhibit the proliferation of PC12 cells and reduce the phosphorylation of ERK may be one of its important molecular mechanisms.