雷公藤甲素对离体子宫内膜癌细胞株增殖及凋亡信号通路PI3K/PKB的影响

The effect of triptolide on proliferation and apoptosis signal transduction pathway-PI3K/PKB in human endometrial carcinoma cell line

目的:探讨雷公藤甲素对人子宫内膜癌细胞株HEC-1B增殖和凋亡的影响,初步探讨其与凋亡信号通路磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(PKB)的关系。方法:观察PI3K/PKB通路抑制剂(LY294002)对雷公藤甲素致子宫内膜癌细胞株HEC-1B凋亡的影响;四甲基偶氮唑盐(MTT)法检测雷公藤甲素对细胞增殖的减轻情况;Western blot观察HEC-1B的PKB磷酸化蛋白表达。结果:MTT实验显示PI3K/PKB通路抑制剂能明显减轻雷公藤甲素对HEC-1B细胞生长的抑制作用,呈浓度依赖性(P<0.05);Western blot结果显示细胞株磷酸化蛋白的表达水平与雷公藤甲素作用浓度呈反比(P<0.05)。结论:雷公藤甲素对子宫内膜癌细胞株HEC-1B的增殖产生抑制作用,并能影响PI3K/PKB信号通路诱导细胞凋亡。

Objective：To investigate the relationship between the effect of triptolide on the proliferation of human endometrial carcinoma cell line（HEC-1B）and the apoptosis related signal transduction pathway-PI3K/PKB.Methods：PI3K/PKB pathway inhibitor（LY294002）was used to detect the effect of triptolide on the apoptosis of HEC-1B.The MTT colorimetry method was performed to measure the inhibitive effect of triptolide on cell proliferation;Western blot was used to observe phosphorylated PKB expression.Results：Result of MTT shows PI3K/PKB pathway inhibitor inhibited the function of TP.The inhibitive effect was related to the drug concentration（P0.05）.Western blot showed the expression of phosphorylated PKB was related to the drug concentration（P0.05）.Conclusion：Triptolide inhibits the proliferation of HEC-1B.The inhibition effect is related to the PI3K/PKB signal transduction pathway.