Elevating miR-378 strengthens the isoflurane-mediated effects on myocardial ischemia-reperfusion injury in mice via suppression of MAPK1.

Objective Myocardial ischemia reperfusion (MI/RI) stresses the pathological process of progressive aggravation of tissue damage in ischemic myocardium. Isoflurane (ISO) is cardioprotective in MI/RI. Thus, this work aimed to identify the mechanism of isoflurane (ISO) post-treatment in MI/RI by regulating microRNA-378 (miR-378) and mitogen-activated protein kinase 1 (MAPK1). Methods A MI/RI model was established by ligating the left anterior descending coronary artery in mice. The modeled mice were injected with ISO or miR-378 or MAPK1 to define their roles in hemodynamics, myocardial injury, cell apoptosis and inflammatory infiltration of mice. CD45, miR-378 and MAPK1 levels were detected. Dual luciferase reporter gene assay was utilized for detection of the targeting connection of miR-378 and MAPK1. Results Reduced miR-378 and elevated MAPK1 existed in MI/RI. ISO elevated miR-378 to target MAPK1. ISO improved hemodynamics and myocardial injury, reduced apoptosis rate and inflammatory infiltration in MI/RI mice. Up-regulated miR-378 further enhanced the protective effect of ISO on MI/RI mice. Depleting MAPK1 reversed the effects of suppressed miR-378 on MI/RI. Conclusion This study highlights that elevating miR-378 strengthens the isoflurane-mediated effects on MI/RI in mice via suppressing MAPK1, which provides a potential treatment for MI/RI.