白藜芦醇诱导人肺腺癌A549细胞细胞凋亡及其与p38 MAPK信号途径的联系

摘要

Objective To study resveratrol( Res)-induced apoptosis in human lung cancer A549 cells and relation with mitogen-actived protein kinase( MAPK) signal pathway. Methods Cytotoxicity was analyzed by CCK-8 meth-od. Apoptotic cells were stained with Annexin V-FITC/ PI and were detected by flow cytometry. Protein expres-sions of cleavage of the Caspases (Caspase-1, Caspase-3) and MAPK(p38,p-p38)were detected by Western blot analysis. Results Res inhibited proliferation of A549 cells with IC50 value of (10. 6 ± 1. 2) μmol/L and induced cell apoptosis. Compared with the control group, apoptotic ratio increased rapidly within 24, 36, 48 h after Res (10 μmol/L) treatment. Cleavage of the Caspase-1, Caspase-3 was observed in A549 cells treated with different doses of Res for 48 h. p38, p-p38 were activated. Conclusion Res inhibits proliferation and induces apoptosis of A549 cells. Activation of p38 pathways may be one of its mechanisms.%目的 探讨白藜芦醇( Res)诱导人肺癌A549细胞株凋亡及其与p38 MARK信号通路的联系. 方法 CCK-8 法检测 Res 对人肺癌 A549 细胞增殖抑制作用, Annexin V-FITC/PI双染法检测Res对肺癌A549 细胞凋亡率, Western blot 法检测 Res 对人肺癌 A549 细胞 Caspase 剪切片断(Caspase-1、Caspase-3)表达的影响,及其对丝裂原激活蛋白激酶(MAPK)通路蛋白(p38、p-p38)表达的影响.结果 Res对人肺癌A549细胞株生长呈浓度依赖性的抑制作用,48 h的Res作用肺癌A549的半数抑制浓度( IC50 ) 值为( 10. 6 ±1. 2)μmol/L. 用10 μmol/L Res处理 A549 细胞24、36、48 h,细胞凋亡率较对照组明显增加( P<0. 01 ). Res作用于A549 细胞 48 h 后, Western blot 法检测显示 Caspase-1、Caspase-3蛋白出现断裂片断,p38、p-p38表达亦增高. 结论Res明显诱导人肺癌A549细胞毒作用,诱导A549细胞凋亡,其机制与激活p-p38 MAPK途径有关.