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.