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目的研究4HPR诱导的膀胱癌细胞凋亡,探讨DNA氧化损伤与修复在其中的作用。方法以4HPR处理T24细胞后,检测其生长抑制情况,用荧光分光光度计检测细胞内活性氧(ROS)含量,用流式细胞仪和琼脂糖凝胶电泳检测细胞凋亡情况,用Westernblot法检测DNA修复蛋白XRCC1的表达。结果4HPR能诱导细胞发生凋亡,2.5、5.0、10.0μmolL4HPR引起的凋亡率分别达到1.8%、4.0%和10.5%,在此过程中伴随着细胞内ROS水平升高(最高达到3倍),并使DNA修复蛋白XRCC1的表达下降,使caspase3激活。抗氧化物质维生素C能有效地抑制4HPR引起的ROS升高,并能部分抑制其引起的细胞生长抑制、凋亡及XRCC1蛋白表达的下降。结论ROS的生成并造成DNA损伤可能是4HPR诱导膀胱癌细胞凋亡的主要机制。
Objective To investigate the apoptosis of bladder cancer cells induced by 4HPR and to explore the role of DNA oxidative damage and repair in it. Methods The growth inhibition of T24 cells was detected by 4HPR. The content of reactive oxygen species (ROS) in cells was detected by fluorescence spectrophotometer. The apoptosis of T24 cells was detected by flow cytometry and agarose gel electrophoresis. DNA repair protein XRCC1 expression. Results 4HPR induced cell apoptosis. The apoptosis rates induced by 2.5, 5.0 and 10.0 μmol L4HPR were 1.8%, 4.0% and 10.5% respectively. During this process, the intracellular ROS level increased up to 3 times, And the expression of DNA repair protein XRCC1 decreased caspase3 activation. Antioxidant vitamin C can effectively inhibit 4HPR caused by increased ROS, and can be partially inhibited by its inhibition of cell growth, apoptosis and XRCC1 protein expression decreased. Conclusion ROS generation and DNA damage may be the main mechanism of 4HPR-induced apoptosis in bladder cancer cells.