AIM To study the effects of κ-opioid receptors on myocardial damage mediated by diabetic mellitus and its underlying mechanism.
METHODS C57BL/6J mice were randomly divided into three groups: a control(Con) group, a diabetic mellitus (DM) group, and DM+U50, 488H (a κ-opioid receptor selective agonist) group. Diabetic mellitus models were established by intraperitoneal injection of streptozotocin (150 mg/kg) and a high fat diet for 7 weeks. Mice in the DM + U50, 488H group were treated with U50, 488H (1.5 mg/kg, i.i) for 1 wk. General physical signs were recorded during the experiment. Fasting blood glucose (FBG) was measured by glucometer and serum insulin was detected by kit. The structure and function of the heart were measured by echocardiography. Myocardial apoptosis was detected by a TUNEL kit and indexes of oxidative stress were measured by Elisa kit.
RESULTS Compared with the Con group, FBG was increased (P < 0.01), wheras serum insulin was decreased significantly (P < 0.01). MDA activity in serum and myocardium were increased (P < 0.01). Total antioxidants content (T-AOC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH) activity (or content) were decreased significantly (P < 0.01). There was an increased myocardial apoptosis (P < 0.01) and a decreased cardiac function in the DM group (P < 0.01). After treatment with U50, 488H, the above effects were abrogated (P < 0.01), which was accompanied by a decreased myocardial apoptosis (P < 0.01) and an increased cardiac function in the DM+U50, 488H group (P < 0.01).
CONCLUSION κ-opioid receptor activation ameliorates myocardial damage caused by diabetic mellitus and further study is needed to demonstrate whether the role of κ-opioid receptor activation is mediated or modulated by inhibiting oxidative stress and improving activity of antioxidants.
DownLoad: