摘要
目的探讨多西紫杉醇（docetaxel，DTX）对人肝癌细胞诱导凋亡的作用及其机制。方法人肝癌细胞株HepG2和Huh7用于实验。通过WST-1细胞增殖实验观察DTX对细胞生长的抑制作用，采用Hoechst33342荧光染色和DNA凝胶电泳检测细胞的凋亡情况，采用Western印迹法检测DTX对Caspase-3和Caspase-9酶原的激活作用。结果DTX对HepG2和Huh7的生长有明显的抑制作用；经Hoechst33342荧光染色和DNA凝胶电泳检测发现DTX可诱导HepG2和Huh7细胞凋亡；在DTX诱导肝癌细胞凋亡的过程中，凋亡效应分子Caspase-3和Caspase-9酶原被剪切激活；Caspase-3抑制剂Z-VAD-FMK抑制DTX诱导的肝癌细胞凋亡。结论DTX对肝癌细胞具有较强的增殖抑制作用，凋亡是其抑瘤的机制之一。DTX导致肝癌细胞凋亡程序依赖于激活Caspase-3酶原途径。
Objective To investigate the effect of docetaxel on the proliferation and apoptosis of human hepatocellular carcinoma cells and explore the mechanism of docetaxel-induced apoptosis. Methods Human hepatoma cells HepG2 and Huh7 were treated with different concentrations of docetaxel for different times, and the proliferation of these cells were examined by WST-1 proliferation assay. Hoechst 33342 staining and DNA ladder were used to detect cell apoptosis. The activities of caspase-3 and caspase-9 were investigated by Western blotting. Results Docetaxel inhibited proliferation of hepatoma cells in a dose-and time-dependent manner. Furthermore, DNA ladder formation and fragmented nuclei were showed in hepatoma cells after docetaxel treatment, indicating that docetaxel induced apoptosis in these cells. Moreover, docetaxel induced caspase-3 and caspase-9 activation. And a caspase-3 inhibitor, Z-VAD-FMK, significantly inhibited docetaxel-induced apoptosis in these hepatoma cells. Conclusions Docetaxel suppresses the proliferation of hepatoma cells through inducing apoptosis and the activated caspase-3 might play an important role in this process.
出处
《中华肝胆外科杂志》
CAS
CSCD
2008年第12期901-903,共3页
Chinese Journal of Hepatobiliary Surgery
基金
基金项目：本课题受国家自然科学基金（资金编号30572114）资助
关键词
癌
肝细胞
多西紫杉醇
细胞凋亡
Carcinoma hepatocellular
Docetaxel
Apoptosis
