磷酸化JNK介导大肠杆菌诱导人巨噬细胞系U937细胞凋亡

Phosphorylated JNK mediated apoptosis induced by E.coli in human U937 cells

目的研究大肠杆菌(Escherichia coli,E.coli)诱导人巨噬细胞系U937细胞凋亡的机制以及特异性c-jun氨基末端激酶(JNK)抑制剂SP600125的保护作用。方法分别用台盼蓝染色和PI标记流式细胞仪检测E.coli感染不同时间后U937细胞的死亡率及凋亡率;Western blot方法分析JNK信号转导通路的激活情况。结果E.coli可诱导U937细胞凋亡,并且具有时间依赖性,此凋亡过程可被JNK的阻断剂SP600125阻断;在此过程中,JNK在E.coli感染10min和20min时被激活并磷酸化。结论E.coli诱导的U937细胞凋亡依赖JNK信号转导通路;SP600125通过特异性地抑制JNK活性降低E.coli诱导的U937细胞凋亡率。

[Objective] To investigate the mechanism of E.coli induced U937 cell apoptosis and the effect of SP600125, a specific c-jun NH2-terminal protein kinase （JNK） inhibitor. [Methods] Apoptosis rates were examined by trypan blue stain and PI stain respectively. The phosphorylated JNK signaling pathway was analyzed by Western blot. [Results] E.cols could invuce U937 apoptosis in a time-dependent manner.SP600125, a JNK blocker, blocked the apoptosis. JNK was phosphorylated at 10min and 20 min. [Conclusion ] E.coli can induce the apoptosis of U937 cells by phosphorylation of JNK. SP600125 protects U937 cells from apoptosis induced by E.coli via inhibiting the activity of JNK.