Cardioprotective Mechanism Of Heme Oxygenase-1 In Rat Cardiomyocytes Subjected To Anoxia-reoxygenation

ObjectiveAcute myocardial infarction(AMI) is an important type of cardiovascular disease, which is severely dangerous to human' s health. Thrombolytic therapy, percutaneous transluminal intervention(PCI) and other revascularization therapies can ameliorate the prognosis of patients with AMI, but these therapies also can lead to ischemia-reperfusion injury, and lower the therapeutic effects. Consequently, the study of protective factors in myocardial ischemia-reperfusion injury has been and is a hot spot in the world. Heme oxygenase is the rate-limiting enzyme in the heme catablization into equimolor biliverdin, carbon monoxide and free iron. There are three isoforms of H0:H0-1,H0-2 and H0-3. H0-1 is the inducible isoform, H0-2 and H0-3 are structural isoforms. H0-1 can be induced by ischemia-reperfusion, heme, heat stress, hypoxia and so on.In recent years, some research found that HO-1 showed obviously protective effects on myocardial ischemia-reperfusion injury,but the specific mechanisms of this cardioprotection have not been elucidated in cardiocytes. In primary cardiomyocytes, we used anoxia-reoxygenation model to mimic myocardial ischemia-reperfusion injury, evaluated the expression of H0-1 mRNA and protein after anoxia-reoxygenation and detected the activity of NF- κB and apoptosis rate to explore the mechanisms of H0-1 in cardioprotection. Methods...