Protective effects of quercetin on mitochondrial oxidative stress in isoproterenol induced myocardial infarcted rats: An in vivo and in vitro study

Abstract

Mitochondrial oxidative stress plays an important role in the pathology of myocardial infarction. The protective effects of quercetin on mitochondrial oxidative stress in isoproterenol induced myocardial infarcted rats were studied. Rats were pretreated with quercetin (10mg/kg body weight) daily for a period of 7days. After the pretreatment period, isoproterenol (100mg/kg body weight) was subcutaneously injected into rats at an interval of 24h for 2days to induce myocardial infarction. Significantly (P<0.05) increased activities/levels of serum creatine kinase, lactate dehydrogenase, heart mitochondrial lipid peroxidation and significantly (P<0.05) decreased activities/levels of mitochondrial antioxidants, tricarboxylic acid cycle and respiratory chain enzymes were observed in isoproterenol induced myocardial infarcted rats. Quercetin pretreatment significantly (P<0.05) decreased the activities/levels of serum creatine kinase, lactate dehydrogenase, heart mitochondrial lipid peroxidation products and significantly (P<0.05) increased the activities/levels of mitochondrial antioxidants. It also restored the activities of tricarboxylic acid cycle and respiratory chain enzymes to near normal in myocardial infarcted rats. Transmission electron microscopic findings confirmed the protective effects of quercetin. The in vitro study on the effect of quercetin on scavenging 1, 1-diphenyl-2-picrylhydrazyl radical also confirmed the free radical scavenging property of quercetin. The possible mechanisms of quercetin on cardiac mitochondrial oxidative stress might be due to decreasing mitochondrial lipid peroxidation, increasing mitochondrial antioxidants and mitochondrial marker enzymes. Thus, quercetin protected rat's heart mitochondria against isoproterenol induced oxidative stress in vivo in myocardial infarction.