五味子乙素诱导人肺癌A549细胞凋亡的机制研究

Inhibitory effect of Schisandrin B on proliferation of lung cancer A549 cells and its mechanism

目的研究五味子乙素(Schisandrin B)对人肺癌A549细胞增殖的抑制作用及其机制。方法将体外培养的肺癌A549细胞分为对照组、五味子乙素组(依五味子乙素浓度不同分为3个亚组),MTT法测定细胞增殖率,流式细胞仪测定细胞凋亡率,Hoechst 33258核染色法观察细胞核凋亡,蛋白免疫印迹法检测肺癌A549细胞内促凋亡信号分子Bax及抗凋亡信号分子Bcl-2的蛋白表达。结果 MTT法检测结果显示,肺癌A549细胞增殖率随五味子乙素浓度的升高而下降(P<0.05);流式细胞仪及Hoechst 33258核染色法的检测结果表明,肺癌A549细胞凋亡率与五味子乙素浓度呈剂量依赖性递增,五味子乙素低、中、高浓度组细胞凋亡率分别为(18.67±3.93)%、(33.33±4.41)%和(49.34±4.70)%,与对照组(3.66±1.90)%比较,差异均有统计学意义(P<0.05);Western blot结果显示,五味子乙素促进了肺癌A549细胞中Bax的表达,抑制了Bcl-2的表达,五味子乙素低、中、高浓度组细胞中Bax、Bcl-2的相对表达量与对照组比较差异均有统计学意义(P<0.05)。结论五味子乙素通过改变线粒体凋亡相关信号分子Bcl-2及Bax的表达,促进肺癌A549细胞凋亡的发生。

Objective To study the inhibitory effect of Schisandrin B on proliferation of lung cancer A549 cells and its mechanism. Methods In vitro cultured lung cancer A549 cells were divided into control group and Schisandrin B group(three different subgroup were divided according to the concentrations of glycoside). Cell proliferation were determined by MTT method, cell apoptosis rate was measured by flow cytometry, nucleus apoptosis was detected by Hoechst 33258 nuclear staining, and protein expressions of Bax and Bcl-2 were detected by Western blot. Results MTT results showed that lung cancer A549 cells’ proliferation rate decreased with the increasing concentration of Schisandrin B(P<0.05);Flow cytometry and Hoechst 33258 nuclear staining test results showed that the apoptosis rate of lung cancer A549 cells increased in a dose-dependent manner with the concentration of schisandrin B increasing, the apoptotic rate of low, medium and high concentration Schisandrin B group were(18.67±3.93)%,(33.33±4.41)% and(49.34±4.70)% respectively, which was significantly different from those of control group(3.66±1.90)%, P<0.05;Western blot showed that Schisandrin B promoted the expression of signaling molecule Bax and inhibited the expression of antiapoptotic signal molecule Bcl-2, the relative expression of Bax and Bcl-2 between the low, medium and high concentration group of Schisandrin B and the control group were significant(P<0.05). Conclusion Schisandrin B could promote lung cancer A549 cells’ apoptosis by changing the expression of mitochondrial apoptosis related signaling molecules Bax and Bcl-2.