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20-HETE Induce ROS Production Exacerbate Myocardial Ischemia Reperfusion Injury

Posted on:2013-07-26Degree:MasterType:Thesis
Country:ChinaCandidate:H TangFull Text:PDF
GTID:2234330395971474Subject:Physiology
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20-Hydroxyeicosatetraenoic acid (20-HETE), a ω-hydroxylation product ofarachidonic acid catalyzed by cytochrome P4504A (CYP4A). The production of20-HETE is increased during ischemia-reperfusion and inhibition of20-HETEproduction has been shown to reduce infarct size caused by ischemia. Our previousstudies show that20-HETE stimulates NADPH oxidase-derived superoxideproduction via a PKC-dependent mechanism in cardiomyocytes. This study aimedat discovering the molecular mechanism underlining the action of20-HETE duringischemia-reperfusion, and the main findings are showed below:⑴The intraceelllarROS content is detected by Dihydroethidium-Superoxide anion fluorescent detectingprobe.⑵By spectrophotometric method for the determination of cardiac tissuehomogenate supernatant of MDA,20-HETE significantly increased ROS and Lipidperoxidation by21%and20%respectively.⑶The RT-PCR results show that20-HETE compared to IR, myocardial cells in NADPH oxidase subunit Nox2mRNAexpression were increased by76%. In summary,20-HETE could contribute to thecardiac injury during myocardial ischemia.
Keywords/Search Tags:isolated rat heart, ischemia reperfusion, ROS, lipid peroxidation, Nox2oxidase
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