| Objective:To investigate the effects of adiponectin to proliferation and the expression of Caspase-3 and T-cadherin in human cardiac myocytes cultured with high glucose,in order to reveal the protective mechanism to human cardiac myocytes of adiponectin and the interrelation of adiponectin and T-cadherin in diabetic cardiomyopathy.Methods:①The human cardiac myocytes were divided into 3 groups in random:normal glucose group(5.5 mmol/L glucose),high glucose group(30mmol/L glucose) and high glucose plus adiponectin group(30mmol/L glucose+2.5μg/ml adiponectin).②Cultured in 24h,48h,72h respectively under the above-mentioned conditions.③To detect the effect of HCM-proliferation by observed the OD in different time and cells with MTT.④Detect the amount of caspase-3 in supernate of HCM collected in diffent time by enzyme-linked immunosorbent assay (ELISA).(5)Extract total RNA in each group cells and synthetic cDNA by reverse transcription,add primer and probe,detct the expression of T-cadherin by Real-Time PCR.Results:1.Compared with normal glucose group,the proliferation of human cardiac myocytes was inhibited in high glucose group,but the proliferation of human cardiac myocytes was promoted after addtion of adiponectin, respectively (P< 0.05)2.The expression of caspase-3 of human cardiac myocytes in high glucose group compare with normal glucose group was significantly increased, but the expression of caspase-3 was significantly decreased after addtion of adiponectin, respectively (P< 0.05)3.Compared with normal group the expression of T-cadherin was decreased in high glucose group,but increased in adiponectin group respectively (P< 0.05), and they have a time-depending character.Conclusion:The continuing effect of high glucose could inhibit cell proliferation and increase the expression of caspase-3,the adiponectin can rectify high glucose-induced apoptosis of human cardiac myocytes.High glucose makes a drop to expression of T-cadherin of human cardiac myocytes,adiponectin plays a protective effect on myocardial cells by upregulating the T-cadherin expression, provide certain theoretical basis to the clinical treatment of diabetic cardiomyopathy. |
