摘要
目的 观察过氧化物酶体增殖物激活受体γ（PPARγ）的配体罗格列酮（RSG）在体外对鼻咽癌CNE2细胞增殖、凋亡的影响及其作用机制.方法 应用CCK-8比色法检测不同浓度（1、10、20、50、100μM）罗格列酮对鼻咽癌CNE2细胞增殖的影响;流式细胞仪检测细胞凋亡率及分析细胞周期;逆转录PCR法观察Bcl-2、Bax的mRNA表达.结果 鼻咽癌CNE2细胞的凋亡率与罗格列酮浓度呈正相关;G0/G1期细胞比例随着罗格列酮浓度升高增加越显著（P＜0.05）.罗格列酮干预鼻咽癌CNE2细胞后,Bcl-2的mRNA表达在鼻咽癌细胞中下调,而Bax的mRNA及蛋白在鼻咽癌细胞中表达上调.结论 罗格列酮可在体外抑制鼻咽癌细胞生长,导致G0/G1期阻滞,并通过调节Bcl-2和Bax的水平而诱导其凋亡.
Objective To explore the role played by peroxisome proliferation activated receptor gamma （PPARγ） ligand Rosiglitazone （RSG） on the regulation of CNE2 cells proliferative and apoptotic.Methods The effect of cell proliferation was studied by CCK-8.The staining of AnnexinV-FITC and PI were used to analyze CNE2 cells apoptosis and cell cycle in each concentration by flow cytometry.The expression of Bcl-2 and Bax mRNA were investigated by reverse transcription polymerase chain reaction （RT-PCR）.Results RSG could inhibit the proliferation of CNE2 cells in concentration dependent and time dependent which were in positive correlation.Cell cycle was arrested at G0/G1 stage by RSG in a concentration dependent manner.RT-PCR indicated the downregulation of Bcl-2 and the upregulation of Bax in mRNA expression.Conclusion Rosiglitazone inhibited nasopharyngeal carcinoma cells growth in vitro,leading to G0/G1 stage arrest,and inducing apoptosis by regulating Bcl-2,Bax levels.
出处
《国际医药卫生导报》
2015年第16期2346-2349,共4页
International Medicine and Health Guidance News
关键词
罗格列酮
鼻咽癌
增殖
凋亡
Rosiglitazone
Nasopharyngeal carcinoma
Proliferation
Apoptosis
