【摘要】 目的:探讨三氧化二砷(As2O3)诱导肝癌细胞凋亡时survivin基因表达和端粒酶活性的变化。方法:采用倒置相差显微镜观察细胞形态,流式细胞仪分析细胞亚二倍体百分率,逆转录-多聚酶链式反应检测细胞survivin mRNA表达,免疫组织化学染色检测细胞survivin蛋白的表达,端粒酶检测试剂盒检测端粒酶活性。结果:0.25~2.00μmol/L As2O3明显抑制肝癌Bel-7402细胞生长,诱导细胞凋亡,survivin mRNA和蛋白表达上调,端粒酶活性下降,呈时间、剂量依赖关系。结论:As2O3抑制肝癌Bel-7402细胞增殖,诱导细胞凋亡,可能与其降低端粒酶活性有关;而survivin基因表达上调,可能是抵抗As2O3诱导凋亡的途径之一。更多还原

【Abstract】 Objective:To explore the changes ofsurvivingene expression and telomerase activity during apoptosis of hepatoma cell lines induced by arsenic trioxide.Methods:Cell morphological changes were observed under phase contrast microscope.Per-centage of diploid cells was analyzed by flow cytometry.The expression level of survivin mRNA was measured by reverse tran-scription polymerase chain reaction(RT-PCR) and survivin protein level was determined by immunohistochemistry.The telom-erase activities were detected using the quantitative telomerase PCR ELISAPLUSR○ kit.Results:Arsenic trioxide 0.25-2.00 μmol/L markedly inhibited growth of hepatoma Bel-7402 cells,induced apoptosis,up-regulated expression of survivin mRNA and protein,reduced telomerase activity in a time-and dose-dependent manner.Conclusion:Arsenic trioxide significantly inhibited the growth of Bel-7402 cells and induced apoptosis,which may be correlated with decrease in telomerase activity.Up-regulation of survivin gene expression was one of the factors that resist arsenic trioxide-induced apoptosis.更多还原