Abstract: Objective To investigate the inhibitory effect of DDAH2 on the apoptosis induced by hypoxia in rat cardiomyocytes through phosphorylation of eNOS. Methods Cell apoptosis was induce by hypoxia within 36hour and was determined by wst-1 and flow cytometry. The phosphorylation of eNOS was examined by western-blot. Results Survival rate of hypoxia group was significantly decreased compared with control group; overexpression DDAH2 induces survival of myocardial cells markedly. After transfection of DDAH2 gene to cardiomyocytes, hypoxia-induced apoptosis significantly declined (17.38%±1.52% vs 27.34%±1.33%, P<0.05). DDAH2 gene transfection significantly increased level of phosphorylation of eNOS in hypoxia of myocardial cells. eNOS inhibitor, L-NAME alleviated the anti-apoptosis effect of overexpression-DDAH2 significantly in H9c2(2-1).Conclusion Overexpression DDAH2 inhibits the apoptosis effects of hypoxia on rat cardiomyocytes H9c2 (2-1) by upregulation of phosphorylation of eNOS.

Key words: DDAH-2, hypoxia, cardiomyocytes, apoptosis