Abstract
ObjectivesDiabetic cardiomyopathy (DCM), characterized by myocardial structural and functional changes, is an independent cardiomyopathy that develops in diabetic individuals. The present study was sought to investigate the effect of curcumin on modulating DCM and the mechanisms involved.MethodsAn experimental diabetic rat model was induced by low dose of streptozoticin(STZ) combined with high energy intake on rats. Curcumin was orally administrated at a dose of 100 or 200 mg·kg−1·d−1, respectively. Cardiac function was evaluated by serial echocardiography. Myocardial ultrastructure, fibrosis area and apoptosis were assessed by histopathologic analyses. Metabolic profiles, myocardial enzymes and oxidative stress were examined by biochemical tests. Inflammatory factors were detected by ELISA, and interrelated proteins were measured by western blot.ResultsRats with DCM showed declined systolic myocardial performance associated with myocardial hypertrophy and fibrosis, which were accompanied with metabolism abnormalities, aberrant myocardial enzymes, increased AGEs (advanced glycation end products) accumulation and RAGE (receptor for AGEs) expression, elevated markers of oxidative stress (MDA, SOD, the ratio of NADP+/NADPH, Rac1 activity, NADPH oxidase subunits expression of gp91phox and p47phox ), raised inflammatory factor (TNF-α and IL-1β), enhanced apoptotic cell death (ratio of bax/bcl-2, caspase-3 activity and TUNEL), diminished Akt and GSK-3β phosphorylation. Remarkably, curcumin attenuated myocardial dysfunction, cardiac fibrosis, AGEs accumulation, oxidative stress, inflammation and apoptosis in the heart of diabetic rats. The inhibited phosphorylation of Akt and GSK-3β was also restored by curcumin treatment.ConclusionsTaken together, these results suggest that curcumin may have great therapeutic potential in the treatment of DCM, and perhaps other cardiovascular disorders, by attenuating fibrosis, oxidative stress, inflammation and cell death. Furthermore, Akt/GSK-3β signaling pathway may be involved in mediating these effects.
Highlights
Diabetes mellitus (DM) has been recognized as a major health problem
Previous studies demonstrated that hyperglycemia, lipid accumulation, excessive generation of reactive oxygen species, cardiac inflammation, accumulation of cardiac fibrosis, and apoptosis are all probably involved in the pathophysiology of Diabetic cardiomyopathy (DCM) [2,4]
Induction of Experimental Diabetes on Rats Experimental diabetic rats were induced by feeding with high fat diet (HFD) during the whole experimental period, whereas rats consuming basal diet (BD) at the same time served as a control group
Summary
The number of diabetic patients worldwide is increasing very fast and expected to reach 439 million by 2030 [1]. The leading cause of death in diabetic patients is cardiovascular disease, which are responsible for the three quarters of the deaths among this population [2]. Diabetic cardiomyopathy (DCM), as an independent diabetic cardiac complication, is characterized by the myocardial dysfunction in the absence of coronary artery disease, hypertension, or valvular heart disease. It has symptoms of early-onset diastolic and lateonset systolic dysfunction [3], which is associated with both type 1 and type 2 DM. The development of DCM has been poorly understood and the mechanisms underlying have not been completely elucidated
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
