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.
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