雷公藤甲素诱导人肺腺癌A549细胞凋亡机制的研究

Mechanism of triptolide induced apoptosis in A549 lung cancer cells

目的:探讨雷公藤甲素(TP)诱导肺腺癌A549细胞凋亡的机制。方法:体外细胞培养,待细胞处于对数生长期时加入4.0μg/mLTP处理24和48h;Western blot检测Sur-vivin、Bcl-2和Fas蛋白质表达;Caspase检测试剂检测Caspase-3和Caspase-9活性。结果:4.0μg/mLTP呈时间依赖性降低Survivin和Bcl-2的表达(与对照组比较P<0.05),升高Fas的表达(与对照组比较P<0.05),TP作用后Caspase-3和Caspase-9活性增强,作用24、48h后Caspase-3活性分别为1.32±0.07和1.46±0.03,Caspase-9活性分别为2.36±0.06和2.41±0.03,与对照组比较,P<0.01。结论:降低Survivin和Bcl-2表达,促进Fas表达可能是TP诱导A549细胞凋亡的机制之一。

OBJECTIVE：To study the mechanism of triptolide induced apoptosis in A549 human lung cancer cells. METHODS： The cells were cultured in vitro, and then were treated with 40 μg/mL TP for 24 and 48 hours. the levels of Survivin, Bcl-2 and Fas were measured by Western-blot. The activities of caspase-3 were assayed with Caspase Colorimetric Assay Kit. RESULTS： Triptolide down-regulated Survivin and Bcl-2 expressions and up-regulated Fas expression in a time-dependent way at 4.0 μg/mL in A549 cells, P〈0.05. The activation of Caspase-3,9 was siginificant increased in A549 cells when exposed to triptolide （4.0 μg/mL） for 24 and 48 hours. The activations of Caspase-3 and Caspase-9 were 1.32±0.07, 1.46±0.03 and 2.36±0.06, 2.41±0.03, respectively and compared with control group, P〈0.01. CONCLUSION：Down-regulation Survivin and Bcl-2 expressions and up-regulation Fas expression could be one of molecular mechanism for triptolide to induce the apoptosis of A549 cells.