miRNA-34a对无血清培养诱导心肌细胞凋亡的影响及机制研究  

Effect of miRNA-34a on serum-free-induced apoptosis in cardiomyocytes and its mechanism

作　　者：邢大伟[1] 张鑫[1] 杨鹏麟[1] 

机构地区：[1]温州医科大学附属第二医院心内科,325027

出　　处：《浙江医学》2014年第21期1779-1781,共3页Zhejiang Medical Journal

摘　　要：目的探讨miRNA-34a(miR-34a)对无血清培养诱导的大鼠心肌细胞凋亡及B淋巴细胞瘤-2基因(Bcl-2)表达水平的影响。方法体外培养大鼠心肌细胞H9C2,实验分实验组(转染miR-34a inhibitor)、空白对照组(无转染miR inhibitor)和阴性对照组(转染随机合成NC microRNA片段)。转染24h后无血清培养饥饿诱导细胞凋亡,Western bolt法检测Caspase-3及Bcl-2的表达。结果实验组细胞Caspase-3表达低于空白对照组和阴性对照组(P<0.05)。Bcl-2表达明显高于空白对照组和阴性对照组(P<0.05)。结论转染miR-34a inhibitor可以下调miR-34a的表达,减少无血清培养诱导H9C2细胞的凋亡,Bcl-2的表达增加可能参与了其保护机制。Objective To investigate the effect of microRNA- 34a （miR- 34a） on serum- free- induced apoptosis in car-diomyocytes and its mechanism. Methods Rat cardiomyocytes H9C2 were cultured in vitro and divided into three groups： in experimental group H9C2 cel s were transfected with miR- 34a inhibitor, blank control group had no transfection, in negative con-trol group cel s were transfected with randomly synthesised miRNA. H9C2 cel s were cultured in serum- free medium to induce apoptosis after transfection. Western blot was preformed to examine the expression of Caspase- 3 and Bcl- 2 protein. Results Western blot showed that compared with blank control and negative control groups, the expression of Caspase- 3 was signifi-cantly decreased in experimental group （P〈0.05）, while the expression of Bcl- 2 was significantly increased in the experimental group（P〈0.05）. Conclusion Transfection of miR- 34a inhibitor down- regulates miR- 34a expression, and inhibites serum- free-induced apoptosis in H9C2 cel s, which is associated with the up- regulation of Bcl- 2.

关 键 词：H9C2 miRNA-34a 凋亡 BCL-2 

分 类 号：R542.2[医药卫生—心血管疾病]