动物实验,II型糖尿病 z-bo 2020-09-03 378

　　OBJECTIVE: To observe the protective effect of GDF11 on myocardial injury in type 2 diabetic C57BL/6J mice and the changes in myocardial cell apoptosis.

　　Method: 60 C57BL/6J male mice weighing 20-25g were randomly divided into 3 groups: normal control group (control group), type 2 diabetes model group (DM), GDF11 intervention group (DM). + GDF11). After feeding on a high-fat, high-sugar diet for 4 weeks, three consecutive intraperitoneal injections of 60 mg/kg streptozotocin (STZ) were given to establish a mouse model of type 2 diabetes. After feeding on a high-fat and high-sugar diet for 4 weeks, the small animals were examined by ultrasound. Collect the myocardial function of the heart tissue, and use TUNEL staining to detect the apoptosis rate of myocardial tissue and cells. The expression of cleaved caspase-3, Bcl-2 and Bax proteins was detected by Western blot.

　　Result: Administration of recombinant GDF11 protein can significantly improve heart function and reduce cardiomyocyte apoptosis, while diabetic injury can significantly reduce left ventricular ejection fraction and left ventricular short axis shortening rate. Increase the rate of cardiomyocyte apoptosis.

　　Conclusion: Exogenous GDF11 can significantly reduce cardiomyocyte apoptosis and improve cardiac function after diabetic injury.