The Mechanism Of Quercetin Against Cardiomyocytes Anoxia/Reoxygenation Injury

Objective:Quercetin, the most abundant of flavonols in food, had been confirmed to protect cardiomyocytes from cardiomyocytes anoxia/reoxygenation injury. Protein kinase Cε (PKCε) was the important endogenous myocardial protective factor. In this study, we established the cultured neonatal rat primary myocardiocytes with the acute myocardial A/R injury model to explore the relationship between the protective effect of quercetin against cardiomyocytes anoxia/reoxygenation injury and the PKCε signal pathway.Method:The cultured neonatal rat primary myocardiocytes were randomly divided into four groups, each group repeated six times:(1)Control group; (2) A/R group; (3) Que+A/R group; (4) Que+εV1-2+A/R group. The cell viability was detected by MTT, and Western blotting analysis assayed the expression of PKCε. The content of MDA and the activities of SOD, LDH, and GSH-Px were analyzed by an automatic biochemical analyzer. Flow cytometry method detected the level of intracellular reactive oxygen species ROS, the mitochondria membrane potential and the percentage of apoptosis.Results:The expression of PKCε protein after preprocessing 40μM quercetin group was significantly raised compared with the control and A/R group (p<0.01); After Que+A/R, the cell viability was increased, the content of MDA was decreased, the activities of SOD and GSH-Px were increased and LDH was decreased, the generation of ROS was decreased, the mitochondria membrane potential were increased, and the apoptosis was decreased,compared with A/R group, and all indicators were significant differences (p<0.01); All indicators were significant differences between Que+A/R group and Que+εV1-2+A/R group (p<0.01), but no significant differences between A/R group and Que+εV 1-2+A/R group (p>0.05)Conclusion:The protective effect of quercetin against cardiomyocytes anoxia/reoxygenation injury at least partly depend on upregulating the expression of PKCε protein.