Emodin Protects against Diabetic Cardiomyopathy by Regulating the AKT/GSK-3[beta] Signaling Pathway in the Rat Model

• Published in: Molecules (Basel, Switzerland) Switzerland), 2014-09, Vol.19 (9), p.14782
• Main Authors: Wu, Zhiqin, Chen, Qingwei, Ke, Dazhi, Li, Guiqiong, Deng, Wei
• Format: Article
• Language: English
• Subjects: Cardiomyopathy; Cardiovascular disease; Diabetes; Fasting; Glucose; Heart failure; Insulin; Metabolic disorders; Oxidative stress
• ISSN: 1420-3049
• DOI: 10.3390/molecules190914782

Diabetes mellitus (DM) has been recognized as a major health problem. Emodin (Emo) has been reported to exhibit protective effects against diabetic nephropathy. However, little has been known about the effect of Emo on diabetic cardiomyopathy (DCM). A type 2 DM model was induced in rats by low dose streptozotocin (STZ) combined with high energy intake. We found that Emo-treated groups displayed significantly higher body weight (BW) and lower heart weight (HW)/BW. Furthermore, Emo could significantly decrease blood glucose, total cholesterol (TG) levels, and triglyceride (TC) levels in diabetic rats. Moreover, the Emo-treated group showed a marked increase in heart rate (HR) and showed lower left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular posterior wall thickness (LWPWT), and interventricular septal diastolic wall thickness (IVSD). Emo induced a significant increase in phosphorylation of Akt and GSK-3β in myocardium. These results suggest that Emo may have great therapeutic potential in the treatment of DCM by Akt/GSK-3β signaling pathway.