miR-200a Attenuated Doxorubicin-Induced Cardiotoxicity through Upregulation of Nrf2 in Mice.

摘要: Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) was closely involved in doxorubicin- (DOX-) induced cardiotoxicity. MicroRNA-200a (miR-200a) could target Keap1 mRNA and promote degradation of mRNA, resulting Nrf2 activation. However, the role miR-200a DOX-related cardiotoxicity remained unclear. Our study is aimed at investigating effect on DOX-induced mice. For cardiotropic expression, male mice received an injection adeno-associated virus 9 (AAV9) system carrying or miR-scramble. Four weeks later, a single intraperitoneal DOX 15 mg/kg. In our study, we found that only microRNA significantly decreased DOX-treated H9c2 cells. supplementation blocked whole-body wasting heart atrophy caused by acute injection, levels cardiac troponin I N-terminal probrain natriuretic peptide, improved adult cardiomyocyte contractile function. Moreover, reduced oxidative stress apoptosis without affecting matrix metalloproteinase inflammatory factors with injection. also attenuated injury cell loss vitro. As expected, activated deficiency abolished protection provided benefits chronic model conclusion, protected against via activation signaling pathway. data suggest may represent new cardioprotective strategy