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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 at different 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.