Objective To investigate the apoptosis induced by casticin on human lung cancer A549 cells and the mechanism involved. Methods Human lung cancer A549 cell line was cultured in vitro. The inhibitory effect of casticin on the proliferation of human lung cancer A549 cells was measured by MTT assay. Casticin-induced apoptosis rates of A549 cells were observed by flow cytometry with annexin V/PI fluorescence staining. The cell mitochondrial membrane potential was detected by flow cytometry with the probe of JC1. Cytochromes-c release of mitochondrion and Bax protein expression were analyzed by Western blotting assay. Results The MTT assay showed that casticin had significantly inhibitory effect on the cell proliferation of A549 cells in a concentration-dependent manner. The flow cytometry with annexin V/PI fluorescence staining indicated that the apoptosis rates of A549 cells treated with 10μmol/L casticin for 12,24 and 48h were 22. 39% ,38.66% and 64. 82% respectively. The flow cytometry with the probe of JC-1 indicated that casticin could down-regulate mitochondrial membrane potential of A549 cells. The results of Western blotting assay demonstrated that the cytochromes-c release of mitochondrion increased, and the expression of Bax up-regulated. Conclusion Casticin possesses a significant function to inhibite the proliferation of A549 cells and to induce the apoptosis of A549 cells, which may be due to the association with down-regulating mitochondrial membrane potential and increasing cytochromes-c release and up-regulating the expression of Bax protein.%目的 探讨紫花牡荆素(CAS)诱导人肺癌A549细胞凋亡及其机制.方法 体外培养A549细胞.MTT法测定CAS对A549细胞的增殖抑制作用；Annexin V/PI双染色分析细胞凋亡率；JC-1探针流式细胞术分析线粒体跨膜电位；Western blotting法分析线粒体细胞色素C的释放和Bax蛋白的表达.结果 CAS能抑制人肺癌A549细胞增殖,呈浓度依赖性.Annexin V/PI法检测结果显示10μmol/L CAS作用A549细胞12、24和48h后,凋亡率分别为22.39％、38.66％和64.82％.JC-1探针流式细胞术分析表明,CAS能降低A549细胞线粒体跨膜电位；Western blotting显示CAS能促进线粒体细胞色素C的释放和上调Bax蛋白表达.结论 CAS具有诱导A549细胞凋亡的作用,其作用机制可能与降低细胞线粒体膜电位、增加细胞色素C释放和上调Bax蛋白表达有关.
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