Melatonin protects against streptozotocin-induced diabetic cardiomyopathy through the mammalian target of rapamycin (mTOR) signaling pathway.

Background. Several studies demonstrated that the overexpression of mammalian target of rapamycin (mTOR) signaling protein is associated with cardiomyopathy. However, the effect of mTOR on the heart in hyperglycemic condition is still controversial. Objectives. We aimed to investigate the expression of mTOR and antioxidant enzyme activity in cardiac hypertrophy in rats with streptozotocin-induced diabetes mellitus (DM), and the effects of the melatonin on diabetic cardiomyopathy (DCM). Material and methods. Forty male Wistar rats were used as the experimental animals. The rats were divided into 4 groups (10 animals in each): group 1 (control group), group 2 (ethanol vehicle group), group 3 (iatrogenically DM-induced group), and group 4 (group given melatonin after iatrogenical DM induction). Streptozotocin was injected intraperitoneally to group 3 and 4 to induce experimental type 1 DM. Melatonin was injected intraperitoneally at a dose of 50 mg/kg/day for 56 days to group 4. We investigated expression of mTOR levels in heart muscle fibers of all groups. Laboratory analysis and transthoracic echocardiography were performed. Results. Melatonin increased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), which were reduced due to hyperglycemia. The mTOR expression levels were significantly higher in group 3 (DM group) compared with controls, whereas melatonin treatment significantly decreased the levels of mTOR expression in group 4 (melatonin + DM group). Diabetic rats developed myocardial hypertrophy with preserved cardiac function. Conclusions. Cardioprotective effect of melatonin may reduce damages caused by DM in the heart muscle fibers through the mTOR signaling pathway.