CAJ | 학술논문

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.
목적 관찰과양화물매체증식물격활수체γ(PPARγ)적배체라격렬동(RSG)재체외대비인암CNE2세포증식、조망적영향급기작용궤제.방법 응용CCK-8비색법검측불동농도(1、10、20、50、100μM)라격렬동대비인암CNE2세포증식적영향;류식세포의검측세포조망솔급분석세포주기;역전록PCR법관찰Bcl-2、Bax적mRNA표체.결과 비인암CNE2세포적조망솔여라격렬동농도정정상관;G0/G1기세포비례수착라격렬동농도승고증가월현저(P＜0.05).라격렬동간예비인암CNE2세포후,Bcl-2적mRNA표체재비인암세포중하조,이Bax적mRNA급단백재비인암세포중표체상조.결론 라격렬동가재체외억제비인암세포생장,도치G0/G1기조체,병통과조절Bcl-2화Bax적수평이유도기조망.
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.