title: The effects of quercetin protect cardiomyocytes from A/R injury is related to its capability to increasing expression and activity of PKCε protein.
abstract: Quercetin is a ubiquitous flavonoid found in vegetable foods. Epidemiological and animal studies have reported an inverse association between quercetin intakes and occurrence and development of various cardiovascular diseases. Some researchers have inferred that the mechanisms of quercetin to protect cardiomyocytes from ischemia/reperfusion injury may be involved in modulation of intracellular signal pathways and regulation of proteins expression beyond its antioxidant activity. The aim of this study was to investigate whether quercetin protect cardiomyocytes from anoxia/reoxygenation injury through PKCε pathway. Neonatal rat primary cardiomyocytes were pretreated with quercetin or quercetin plus εV1-2, a selective PKCε inhibitor, prior to A/R treatment. Western blotting analysis showed that the level of PKCε and phosphor-PKCε Ser297 in the quercetin pretreatment group were all increased significantly compared to the control or A/R group. Subsequent assays showed that pretreated with quercetin could increase the viability of neonatal rat primary cardiomyocytes suffered A/R, decrease the apoptosis and ROS and alleviate the loss of mitochondrial membrane potential induced by A/R injury. However, the protective effects of quercetin disappeared in the group pretreated with εV1-2. Thus, for the first time, we revealed that one of the mechanisms of quercetin protecting cardiomyocytes from A/R injury might be increase the expression of PKCε protein and then enhance the activity of its downstream pathway.
authors.affiliation: State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, 330047, People's Republic of China.
authors.forename: Lei
authors.initials: L
authors.lastname: Tang
authors.forename: Yian
authors.initials: Y
authors.lastname: Peng
authors.forename: Tiantian
authors.initials: T
authors.lastname: Xu
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Yi
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Yuchao
authors.initials: Y
authors.lastname: Luo
authors.forename: Dong
authors.initials: D
authors.lastname: Yin
authors.forename: Ming
authors.initials: M
authors.lastname: He
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology*; D015687:Cell Hypoxia / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019610:Cytoprotection / Q000187:drug effects*; D005979:Glutathione Peroxidase / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D010100:Oxygen / Q000494:pharmacology*; D051744:Protein Kinase C-epsilon / Q000378:metabolism*; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D011794:Quercetin; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D051744:Protein Kinase C-epsilon; D010100:Oxygen