Objective: To observe the protective effect of GDF11 on myocardial injury in C57BL/6J mice with type Ⅱ diabetes mellitus and the changes of myocardial apoptosis.
Methods: Sixty male C57BL/6J mice weighing 20-25 g were randomly divided into 3 groups: normal control group (control), type Ⅱ diabetes model group (DM) and GDF11 intervention group (DM+GDF11). After being fed on high-fat and high-sugar diet for 4 weeks, 60 mg/kg streptozotocin (STZ) was injected intraperitoneally for 3 consecutive times to establish a type II diabetic mouse model. Cardiac function was detected, myocardial tissue was collected, TUNEL staining was used to detect the apoptosis ratio of myocardial tissue, and Western blot was used to detect the expression of apoptosis-related proteins cleaved-caspase-3, Bcl-2 and Bax.
Results: Diabetic injury significantly reduced left ventricular ejection fraction and left ventricular short-axis shortening rate, and increased myocardial apoptosis rate, while administration of recombinant GDF11 protein could significantly improve cardiac function and reduce myocardial apoptosis.
Conclusion: Exogenous GDF11 can significantly reduce myocardial apoptosis and improve cardiac function after diabetic injury.