MiR-146a通过抑制TRAF6减轻自身免疫性心肌炎大鼠心脏炎症并改善其心功能  

MiR-146a Ameliorates Myocarditis and Improves the Cardiac Function in EAM Rats by Inhibiting TRAF6

作　　者：赵思嘉[1] 许蔚起[1] 刘娜[1] 王丽君[1] 吴岳[1] 周娟[1] 袁祖贻[1] 

机构地区：[1]西安交通大学第一附属医院心血管内科环境与疾病相关基因教育部重点实验室陕西省分子心脏病学重点实验室,陕西省西安市710061

出　　处：《中国分子心脏病学杂志》2015年第1期1202-1205,共4页Molecular Cardiology of China

基　　金：国家重点基础研究发展计划(973计划:No.2012CB517804);国家自然科学基金资助项目(No.81025002)

摘　　要：目的巨噬细胞浸润并活化是自身免疫性心肌炎(EAM)病理的重要特点,微小RNA(micro RNA,mi RNA)在其发生,发展过程中的作用目前依然不明。本实验探讨在巨噬细胞活化中高表达的mi R-146a在EAM中的作用。方法成功造模的EAM大鼠分别给予Mi R-146a micr ON?mi RNA agomirs(mi R-146a agomirs)和阴性对照试剂,对比其心功能指标及炎症指标变化。结果给予mi R-146a agomirs可以显著降低EAM大鼠心脏炎症并改善其心功能,且该作用是通过直接抑制其靶蛋白肿瘤坏死因子受体相关因子6(TRAF6),进而抑制核因子活化B细胞κ轻链增强子(NF-κB)活化通路来实现的。结论 mi R-146a在体通过抑制TRAF6/NF-κB信号通路改善心肌炎。Objective To investigate the role and the mechanism of miR-146a which is highly expressed in activated macrophages in experimental autoimmune myocarditis （EAM）, as diffusion and activation of macrophages are significant features of EAM. Methods Detection and comparison of the cardiac function and expression level of proinflammatory mediators in EAM rats that administrated with MiR-146a micrONTM miRNA agomirs （miR-146a agomirs） or negative control reagent, respectively. Results By the mechanism that miR-146a could block nuclear factor kappa-light-chain- enhancer of activated B cells （NF-κB） pathway by directly targeting receptor associated factor 6 （TRAF6）, administration of miR-146a agomirs could significantly attenuate the myocarditis and improve the cardiac functions. Conclusion miR-146a could ameliorate myocarditis by inhibiting TRAF6/ NF-κB pathway in vivo.

关 键 词：心肌炎 炎症 MIRNA 核因子-ΚB 

分 类 号：R542.21[医药卫生—心血管疾病]