The effects of quercetin protect cardiomyocytes from A/R injury is related to its capability to increasing expression and activity of PKCε protein
| Autor: | Ming He, Ying Liu, Tiantian Xu, Xiaoqing Yi, Yian Peng, Yuchao Luo, Dong Yin, Lei Tang |
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| Rok vydání: | 2013 |
| Předmět: |
Cardiotonic Agents
Antioxidant Cell Survival medicine.medical_treatment Clinical Biochemistry Flavonoid Apoptosis Myocardial Reperfusion Injury Protein Kinase C-epsilon Pharmacology Biology Rats Sprague-Dawley chemistry.chemical_compound Malondialdehyde medicine Animals Myocytes Cardiac heterocyclic compounds Molecular Biology Cells Cultured Membrane Potential Mitochondrial chemistry.chemical_classification Cardioprotection Glutathione Peroxidase L-Lactate Dehydrogenase Superoxide Dismutase Cell Biology General Medicine medicine.disease Cell Hypoxia Rats Oxygen Blot Oxidative Stress Animals Newborn chemistry Biochemistry Cytoprotection Quercetin Reactive Oxygen Species Reperfusion injury Intracellular |
| Zdroj: | Molecular and Cellular Biochemistry. 382:145-152 |
| ISSN: | 1573-4919 0300-8177 |
| DOI: | 10.1007/s11010-013-1729-0 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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