Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion

► IMD1-53 attenuated the myocardial injury by inhibiting MDA content and LDH activity, elevating the Mn-SOD and CAT activity and decreasing the expression of gp91phox and p47phox. ► IMD1-53 attenuated H2O2-induced cardiomyocyte apoptosis in vitro. ► IMD1-53 activated the ERK1/2 signaling pathway. ► IMD1-53 may improve the oxidative stress injury by enhancing ERK phosphorylation.