Remifentanil protects against myocardial ischemia/reperfusion injury via miR-205-mediated regulation of PINK1

Myocardial ischemia/reperfusion (I/R) injury could lead to severe cardiovascular ischemic disease, including myocardial infarction and contractile dysfunction. Remifentanil demonstrated protective effect on I/R injury. The underlying pathophysiological mechanism was then investigated in this study. In the current study, primary cardiomyocytes were isolated from rats, preconditioned with remifentanil. Rats, tail vein injected miR-205 antagomir, subjected infusion of remifentanil, regional ischemia followed by reperfusion. results that cell viability hypoxia/reoxygenation-induced increased post while apoptosis decreased accompanied reduced cleaved caspase-3 expression. Hypoxia/reoxygenation treatment PINK1 (PTEN induced putative kinase 1) However, preconditioning remifentanil enhanced PINK1. Moreover, over-expression expression counteracted effects remifentanil-induced increase decrease cardiomyocytes. Injection antagomir improved infarct size LDH (lactic acid dehydrogenase) activity rat model conclusion, might participate via regulation PINK1, providing a potential target for amelioration disease.