二氢青蒿素对膀胱癌T24细胞株的抑制作用及其机制研究  

Inhibitory effects and mechanisms of dihydroartemisinin on the bladder cancer cell line T24

作　　者：王国强[1] 袁亚光[1] 朱小军[1] 闫骏[1] 

机构地区：[1]内蒙古医科大学附属医院泌尿外科,内蒙古呼和浩特010059

出　　处：《中国医药导报》2013年第3期7-9,共3页China Medical Herald

摘　　要：目的探讨二氢青蒿素体外抗膀胱癌T24细胞株活性及相关机制。方法采用体外培养的T24细胞株为研究对象,流式细胞仪检测二氢青蒿素作用后T24细胞凋亡率,Caspase-3活性检测试剂盒检测Caspase-3活性,免疫印迹法检测细胞凋亡关键蛋白p53、Bax、Caspase-3、Bcl-2的表达变化。结果二氢青蒿素能够诱导T24肿瘤细胞凋亡(P<0.01),且呈剂量-效应关系;二氢青蒿素还可引发T24肿瘤细胞Caspase-3活性水平升高(P<0.05或P<0.01),促凋亡蛋白Caspase-3、Bax高表达(P<0.01),抗凋亡蛋白Bcl-2表达降低(P<0.01),且均呈现时间-效应关系。p53表达水平无显著改变(P>0.05)。结论二氢青蒿素具有明确的抑制膀胱癌T24细胞株的效应,其机制可能是激活非依赖于p53的Bcl-2家族介导的细胞色素C途径,进而引发T24细胞凋亡。Objective To explore the antitumor activities in vitro and mechanisms of dihydroartemisinin.Methods T24 cell line cultured in vitro were used as the objects of study,apoptosis rate of T24 cell was detected by flow cytometry（FCM） analysis,the activity of Caspase-3 was examined by colorimetry,the expression level of p53,Bax,Caspase-3 and Bcl-2 was determined by Western blotting.Results The apoptosis of T24 cell was induced by dihydroartemisinin（P〈0.01）,the dose-effect relationship was seen;the activity and expression level of Caspase-3 and Bax were significantly increased when treated with dihydroartemisinin（P〈0.05 or P〈0.01）;the Bcl-2 was reduced after treatment with dihydroartemisinin（P〈0.01）.However,the expression level of p53 was found no changes（P〈0.05）.Conclusion Dihydroartemisinin has great antitumor activities on the bladder cancer cell line T24,the mechanism most possibly is by triggering cytochrome C apoptotic pathway which mediated by Bcl-2 family.

关 键 词：二氢青蒿素 膀胱癌 p53 BAX CASPASE-3 BCL-2 

分 类 号：R73[医药卫生—肿瘤]