Effects Of Adiponectin On Cell Oxidative Stress And Apoptosis In Human Cardiacmyocytes Cultured With High Glucose

Objective: To establish a myocardial cell oxidative stress model by cultivating HumanCardiacmyocytes (HCM) in a high glucose environment, and to observe if there is a protectiverole of adiponectin (ADPN) on the oxidative stress and apoptosis of myocardial cells, andreveals the may be protection mechanism of the adiponectin.Methods: The in vitro cultured Human Cardiacmyocytes were divided into three groups:the control group, high glucose group, high glucose + adiponectin group, and these cells werecultured 24 h, 48 h, 72 h respectively. Then observe the morphological change of the HCMunder the inverted microscope and evaluated for the level of superoxide dismutase (SOD) by thexanthineoxidase method. The level of malondialdehyde (MDA) was detected by benzodiazepinesacid method. The expression of adaptin (P66Shc) and heme oxygenase-1 (Ho-1) in three timepoints was detected by Real-Time PCR, and the apoptosis rate of human cardiacmyocytes weretested by the Flow Cytometry.Results: Our findings showed significant increase of MDA levels（P＜0.05) anddecrease of SOD activity（P＜0.05) in the high glucose group compared with the controlgroup．However in the adiponectin group MDA levels decreased（P＜0.05) and SOD activityincreased significantly（P＜0.05) compared with those in the high-glucose group and they aretime-dependent. Compared with the control group, the expression of Ho-1 mRNA and P66ShcmRNA increased in the high-glucose group; the adiponectin group expressed a higher level ofHo-1 mRNA but a lower level of P66Shc mRNA compared with the glucose group（P＜0.05)and they are time-dependent. The apoptosis rate of human cardiacmyocytes in the high-glucosegroup is higher than the control group; while the apoptotic rate in the adiponectin group declinedremarkably compared with the high glucose group.Conclusion: The adiponectin has a protective effect on diabetes myocardial cells byupregulating the expression of Ho-1 mRNA and downregulating the expression of P66ShcmRNA, which can increase the antioxidant capacity, reduce oxidative stress and reduce highglucose-induced apoptosis of HCM.