亚砷酸对人肝癌细胞凋亡及Caspase-3活性的影响

Arsenic trioxide induces apoptosis and upregulates Caspase-3 activity in human hepatic carcinoma cells

目的探讨亚砷酸对人肝癌细胞凋亡及半胱氨酸蛋白酶（Caspase）-3活性的影响。方法采用细胞培养技术，以肝癌细胞系SMMC7721为靶细胞，以不同浓度的药物处理细胞72h后，利用WST-8法测定亚砷酸对细胞增殖的影响；利用荧光染料Hoechst33258染色，荧光显微镜观察细胞核碎片；以流式细胞仪分析细胞周期的变化；采用CaspasebE色法检测Caspase-3活性。结果亚砷酸（10umol／L）对SMMC7721细胞有明显抑制作用，可诱导SMMC7721细胞凋亡，并能增强Caspase-3基因的活性。结论亚砷酸能够诱导SMMC7721细胞凋亡，其机制与Caspase-3依赖性凋亡调节信号通路有关。

Objective To investigate the effect of arsenic trioxide （ATO） on apoptosis and Caspase-3 activity of human hepatic carcinoma cell line SMMC7721. Methods SMMC7721 ceils were treated with ATO 10umol/L for 72 h and cell apoptosis was observed microscopically with Hoechst 33258 staining. The proliferation of the cells was detected with WST-8 method. The cell cycle was examined by flow cytometry. The Caspase-3 activity was detected with Caspase-3 colorimetric protease assay. Results Arsenious acid inhibited proliferation of SMMC7721 cells, induced cell apoptosis and upregulated the Caspase-3 activity. Conclusion ATO induces apoptosis of SMMC7721 cells, which may be associated with Caspase-3 pathway.