Effect of hypoxia/reoxygenation on the viability expression of ROS and MAPKs in myocardial cells

摘要

Objective:To investigate to the expression effect of hypoxia and hypoxia/reoxygenation on ROS,MAPKs and cell apoptosis in H9c2 cardiomyocytes.Methods:H9c2 cells were treated with cobalt chloride(CoCl2)to establish the chemical hypoxia and hypoxia/reoxygenation-induced cardiomyocyte injury model.CoCl2 was used to process cells atdifferent concentrations from 150-2400μmol/L and different time from4-24 h;H9c2 cells viability was detected by MTT,and the intracellular ROS level was measured by 2’,7’-dichlorflμoresceindiacetate(DCFH-DA)and dihydroethidiμm(DHE)staining and photoflurography.The active expression level of mitogen-activated protein kinases(MAPKs)(including JNK,ERK and p38)and caspase-3.Results:At the concentration from 300 to 1200μmol/L,CoCl2 does/time-dependently inhibited the cell viability in H9c2 cells(P<0.01).Compared with control group,the ROS levels in hypoxia group were significantly increased(P<0.05).In hypoxia group,the active expression levels of p-JNK,p-p38 and caspase-3 was higher than those in control group(P<0.05).However,the expression of p-ERK wasn’t significant differernce.Furthermore,all the expression levels of ROS,p-JNK,p-ERK,p-p38 and caspase-3 in H/R group were significantly raised compared with hypoxia group(P<0.01).Conclusions:Reoxygenation further aggravate chemical hypoxia induced cardiomyocyte oxidative stress injury by activating ROS/MAPKs signals,suggesting the role of myocardial ischemia/reperfusion injury in the pathogenesis of ischemic heart disease.