百里醌诱导膀胱癌细胞凋亡作用机制的研究
投稿时间:2014-08-24  修订日期:2014-09-16  点此下载全文
引用本文:王大文,朱诗建,木海琦,李晟,周鹏飞,杨森,南存金,陈映鹤.百里醌诱导膀胱癌细胞凋亡作用机制的研究[J].医学研究杂志,2015,44(3):93-96
DOI: 10.3969/j.issn.1673-548X.2015.03.026
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作者单位E-mail
王大文 325000 温州医科大学附属第二医院  
朱诗建 325000 温州医科大学附属第二医院  
木海琦 325000 温州医科大学附属第二医院  
李晟 325000 温州医科大学附属第二医院  
周鹏飞 325000 温州医科大学附属第二医院  
杨森 325000 温州医科大学附属第二医院  
南存金 325000 温州医科大学附属第二医院  
陈映鹤 325000 温州医科大学附属第二医院 chenyh@wzhealth.com 
基金项目:浙江省中医药科技计划基金资助项目(2011ZB092);浙江省卫生厅基金资助项目(2012KYB134)
中文摘要:目的 探讨百里醌对人膀胱癌细胞株BIU-87细胞凋亡的影响及对其诱导凋亡的潜在作用机制。方法 应用CCK8法检测细胞增殖活性, Hoechst33258染色法检测细胞凋亡, 荧光定量PCR检测基因Bcl-2、Bax、caspase-3、c-myc mRNA的表达水平, Wsetern blot法检测不同浓度百里醌作用后Bcl-2、Bax、c-myc蛋白表达水平的变化。结果 细胞增殖抑制曲线结果显示百里醌能明显抑制BIU-87细胞增殖, 其24、48、72h半数抑制浓度(IC50)分别是38.75±0.58、34.33±1.01和32.43±0.71μmol/ L。百里醌能以剂量依赖性方式诱导膀胱癌细胞凋亡。百里醌作用于BIU-87细胞后, Bcl-2、c-myc mRNA及Bcl-2、c-myc蛋白的表达量呈浓度依赖性降低, 而caspase-3、Bax mRNA及caspase-3、Bax蛋白表达水平呈浓度依赖性递增。结论 百里醌能抑制BIU-87细胞的增殖, 且能诱导BIU-87细胞的凋亡, 其诱导凋亡机制可能与Bcl-2、c-myc表达水平降低及caspase-3、Bax表达水平上调有关。
中文关键词:百里醌  膀胱癌  Bcl-2  Bax  c-myc  caspase
 
Effects of Thymoquinone on Inducing Bladder Cancer BIU-87 Apoptosis
Abstract:Objective To investigate the effect of thymoquinone(TQ) on the human bladder cancer cell lines (BIU-87) apoptosis and its possible mechanisms of inducing apoptosis. Methods Cell proliferation ability was calculated by cell counting kit-8(CCK8). Hoechst staining was used to observe the apoptosis of BIU-87 cells, treated with different concentrations of TQ. The mRNA expressions of Bcl-2, Bax, c-myc and caspase-3 were detected by real time fluorescent quantitative PCR. The expressions of Bcl-2, bax and c-myc proteins were determined by Western blot. Results The results showed that TQ remarkably inhibited the BIU-87 cell proliferation with the IC50 of 24h、48h and 72h respectively were 38.75±0.58, 34.33±1.01, 32.43±0.71μmol/L. Apoptosis was induced after treated with TQ. Compared with the blank control group, the mRNA and proteins expressions of Bcl-2 and c-myc obviously decreased in a dose-dependent manner, while the expressions of bax and caspase-3 were upregulated. Conclusion TQ could significantly inhibit the proliferation ability of BIU-87 cells, and also induce apoptosis probably by upregulating the expressions of Bax and caspase-3 and downregulating the expressions of Bcl-2 and c-myc.
keywords:Thymoquinone  Bladder cancer  Bcl-2  Bax  C-myc  Caspase
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