甘草酸对人肺癌细胞A549凋亡及Bcl-2和Bax表达的影响

Effects of glycyrrhizic acid on apoptosis,Bcl-2 and Bax expression of lung adenocarcinoma A549 cells

目的：探讨甘草酸诱导人肺癌细胞A549凋亡作用及机制研究。方法 ：采用噻唑蓝（MTT）法测定甘草酸对A549的生长抑制作用,倒置显微镜观察甘草酸对A549细胞作用后的形态改变,TUNEL实验检测细胞凋亡情况,罗丹明123（Rh123）荧光染色观察线粒体膜电位的改变,免疫印迹实验探讨甘草酸的作用机制。结果：与空白组相比较,不同浓度甘草酸（0.5-4mmol/L）能够抑制A549肺癌细胞增殖并呈时间-浓度依赖性,确定甘草酸最佳作用时间为24 h,最佳作用浓度为1 mmol L。甘草酸（1 mmol/L）作用24 h后能够显著降低细胞线粒体膜电位并能够下调Bcl-2蛋白表达,上调促凋亡蛋白Bax和cytochrome c蛋白表达。结论：甘草酸能够显著抑制A549肺癌细胞增殖并通过线粒体依赖的凋亡途径发挥作用。

Objective： In present study, effects of glyeyrrhizic acid on cell viability and apoptosis were investigated in human non-small cell lung cancer A549 cells. Methods： Treated with various concentrations of glycyrrhizic acid at different time intervals. Apoptotic bodies were observed in the cells by light microscope. The changes of mitochondrial transmembrane potential （△ψm） in the A549 cells were analyzed with rhodamine 123 staining. Western blot analysis was used to evaluate the levels of cytochrome c （cyto c ）, Bax, Bcl-2 expressions. Results： The results showed that glycyrrhizic acid （0.5 - 4mmol/L） induced apoptosis in A549 cells in a dose-dependent manner, as determined by MTY assay, and demonstrated that the proper time and dose is 24 h and 1 mmoL/L, respectively. Glycyrrhizic acid （1 mmol/L） treatment with 24 h significantly reduced △ψm. Further analysis by western blotting showed that the expression of cyto c and Bax were increased, while the expression of antiapoptotic Bcl-2 was increased. Conclusion： Taken together, our results demonstrated that glycyrrhizic acid was capable of inhibiting A.549 cell proliferation and inducing apeptosis via mitochondrial-dependent pathway.