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, the proportion of myocardial tissue apoptosis was detected by TUNEL staining, and the expressions of apoptosis-related proteins cleaved-caspase-3, Bcl-2 and Bax were detected by Western blot.
Results: Diabetic injury significantly down-regulated 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.