Anti-Apoptotic Effect of MicroRNA-30b in Early Phase of Rat Myocardial Ischemia-Reperfusion Injury Model

作者：Song, Chun-Li; Liu, Bin^*; Wang, Jin-Peng; Zhang, Bei-Lin; Zhang, Ji-Chang; Zhao, Li-Yan; Shi, Yong-Feng; Li, Yang-Xue; Wang, Guan; Diao, Hong-Ying; Li, Qian; Xue, Xin; Wu, Jun-Duo; Liu, Jia; Yu, Yun-Peng; Cai, Dan; Liu, Zhi-Xian

来源：Journal of Cellular Biochemistry, 2015, 116(11): 2610-2619.

DOI：10.1002/jcb.25208

• MICRORNA-30B
• ANTI-APOPTOSIS
• ISCHEMIC-REPERFUSION INJURY
• KRAS
• RAS
• AKT PATHWAY
• BCL-2
• BAX
• CASPASE-3

This study aimed to investigate the effect of microRNA-30b (miR-30b) in rat myocardial ischemic-reperfusion (I/R) injury model. We randomly divided Sprague-Dawley (SD) rats (n=80) into five groups: 1) control group; 2) miR-30b group; 3) sham-operated group; 4) I/R group, and 5) I/R+miR-30b group. Real-time quantitative polymerase chain reaction, immunohistochemical staining and Western blot analysis were conducted. TUNEL assay was employed for testing cardiomyocyte apoptosis. Our results showed that miR-30b levels were down-regulated in I/R group and I/R+miR-30b group compared with sham-operated group (both P<0.05). However, miR-30b level in I/R+miR-30b group was higher than I/R group (P<0.05). Markedly, the apoptotic rate in I/R group showed highest in I/R group (P<0.05). Additionally, the results illustrated that protein levels of Bcl-2, Bax, and caspase-3 were at higher levels in ischemic regions in I/R group, comparing to sham-operated group (all P<0.05), while Bcl-2/Bax was reduced (P<0.05). Bcl-2 level and Bcl-2/Bax were obviously increased in I/R+miR-30b group by comparison with I/R group, and expression levels of Bax and caspase-3 were down-regulated (all P<0.05). We also found that in I/R+miR-30b group, KRAS level was apparently lower and p-AKT level was higher by comparing with I/R group (both P<0.05). Our study indicated that miR-30b overexpression had anti-apoptotic effect on early phase of rat myocardial ischemia injury model through targeting KRAS and activating the Ras/Akt pathway. J. Cell. Biochem. 116: 2610-2619, 2015.

• 出版日期2015-11
• 单位吉林大学