Protective effects of urocortin on diabetic cardiomyopathy and relationship via Akt/GSK-3β signaling pathway / 中国药理学通报

ABSTRACT

Aim To observe the effects of UCN on TGF-β1 and CTGF in rats with DCM, and to explore the protective effects of UCN on DCM and its possible signaling pathway. Methods The rats were divided into five groups Control group, DCM group, UCN group, UCN + Astressin group, and UCN + Triciribine group. After 12 weeks of feeding and 4 weeks of treatment, blood glucose, urinary sugar, urine volume and the levels of TGF-β1, CTGF in serum were determined, and the expression of TGF-β1, CTGF, Akt, GSK-3β, p-Akt and p-GSK-βof cardiomyocytes were also determined. Results The myocardial HE staining in DM rats was consistent with DCM. The levels of TGF-β1 and CTGF in serum and myocardium of rats with DCM increased significantly, while the levels of p-Akt and p-GSK-3J3 in myocardium of rats with DCM decreased significantly ( P < 0. 05 ). The levels of TGF-β1 and CTGF in UCN group decreased, both as-tressin and triciribine could inhibit the role of UCN, and the expression of p-Akt and p-GSK-3(3 in myocardial cells in UCN group increased significantly, then astressin could inhibit the role of UCN ( P < 0. 01). Conclusions The protective effects of UCN on DCM might be related to the activation of Akt/GSK-30 signaling pathway after binding with CRH-R receptor, and then decreasing the expression of TGF-β1 and CTGF.