摘要
目的观察辛伐他汀诱导K562细胞凋亡时Bcl-2/Bax变化,探讨Bcl-2/Bax与细胞凋亡之间关系。方法 20μmol/L辛伐他汀处理K562细胞24、48和72h;流式细胞技术检测细胞凋亡率;免疫组织化学法检测细胞色素C,RT-PCR技术检测Bcl-2/Bax基因。结果 20μmol/L辛伐他汀作用K562细胞24、48和72h,细胞凋亡率变化分别是(6.1±0.4)%,(14.2±0.4)%,(30.7±0.6)%;胞浆内细胞色素C显著高于对照组(P<0.05);抑凋亡基因Bcl-2显著降低,促凋亡基因Bax显著升高(P<0.05)。结论辛伐他汀能诱导K562细胞凋亡,Bcl-2/Bax比值降低可能是辛伐他汀诱导K562细胞凋亡机制之一。
Objective To study the changes rate of Bcl-2/Bax in K562 cell at the process of apoptosis induced by simvastatin and presume the relation between Bcl-2/Bax with apoptosis.MethodsK562 cells were exposed to 20μmol/L concentrations of simvastatin in different times（24h,48h and 72h）;Flow cytometry were performed to confirm cell apoptotic ratio;Colorimetric method was used to measure protein of Cyto C;Reverse transcriptase-polymerase chain reaction was used to detect the quantity of gene Bcl-2 and Bax;The expression of Cyto C protein was detected by immunohistochemical method.ResultsK562 cells could undergo apoptosis after the treatment of 20μmol/L simvastatin for 24h,48h and 72h,and the apoptotic ratio are 6.1±0.35%,（14.15±0.42）%,（30.70±0.65）%,respectively.The quantity of protein of cyto C were increased markedly in treated groups detected by immunohistochemical in（P〈0.05）.The mRNA of Bax expression levels in drug-treated group were up-regulated,while the mRNA of Bcl-2 was down regulated.ConclusionK562 cells could be induced to apoptosis by simvastatin,the underlying mechanism might be related to down regulation of Bcl-2 and up regulated of Bax.
出处
《四川医学》
CAS
2011年第6期803-806,共4页
Sichuan Medical Journal
基金
四川省卫生厅科研基金资助(编号:060119)
