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Background Diabetic cardiomyopathy is the major cause of morbidity and mortality in diabetic patients.Oxidative stress plays an important role in diabetic cardiomyopathy.This study aimed to investigate the effects of adiponectin on oxidative stress and apoptosis in human cardiac myocytes (HCM) cultured with high glucose.Methods The cells were assigned to three group: control group,high glucose group and high glucose plus adiponectin group.After culture for 24,48,72 hours,oxidative stress was evaluated by detecting levels of malondialdehyde (MDA)and superoxide dismutase (SOD) in the supatant of culture media.The expression of p66Shc and Heme oxygenase-1 (HO-1) was detected by real-time polymerase chain reaction (PCR).Flow cytometry was designed to observe and detect cellular apoptosis.Results Our findings showed significant increase in MDA levels and decrease in SOD activity in the high glucose group compared with the control group (P ＜0.05).However,MDA levels were significantly decreased and SOD activity was significantly increased in the adiponectin group compared with those in the high-glucose group (P ＜0.05).The mRNA expression of HO-1 in the high glucose group was significantly increased in a time-dependent manner compared with that in the control group (P ＜0.05).Adiponectin further increased the mRNA expression of HO-1 induced by high glucose in a time-dependent manner (P ＜0.05).The expression of p66Shc was significantly increased in high glucose group compared with that in the control group (P ＜0.05).Adiponectin significantly suppressed the upregulation of p66Shc induced by high glucose (P ＜0.05).The apoptotic rate of cardiomyocytes was significantly increased in the high glucose group compared with that in the control group while the apoptotic rate in the adiponectin group was remarkably declined in comparison with that in the high glucose group.Conclusion Adiponectin reduces high glucose-induced oxidative stress and apoptosis and plays a protective role in myocardial cells by upregulating the HO-1 expression and downregulating p66Shc expression.