Abstract
Diabetic cardiomyopathy (DCM) is the principal cause of death in people with diabetes. However, there is currently no effective strategy to prevent the development of DCM. Although cyclovirobuxine D (CVB-D) has been widely used to treat multiple cardiovascular diseases, the possible beneficial effects of CVB-D on DCM remained unknown. The present aim was to explore the potential effects and underlying mechanisms of CVB-D on DCM. We explored the effects of CVB-D in DCM by using high fat high sucrose diet and streptozotocin-induced rat DCM model. Cardiac function and survival in rats with DCM were improved via the amelioration of oxidative damage after CVB-D treatment. Our data also demonstrated that pre-treatment with CVB-D exerted a remarkable cytoprotective effect against high glucose -or H2O2 -induced neonatal rat cardiomyocyte damage via the suppression of reactive oxygen species accumulation and restoration of mitochondrial membrane potential; this effect was associated with promotion of Nrf2 nuclear translocation and its downstream antioxidative stress signals (NQO-1, Prdx1). Overall, the present data has provided the first evidence that CVB-D has potential therapeutic in DCM, mainly by activation of the Nrf2 signalling pathway to suppress oxidative stress. Our findings also have positive implications on the novel promising clinical applications of CVB-D.
Highlights
Diabetic cardiomyopathy (DCM) is the principal cause of death in people with diabetes
Cardiac function parameters were measured by electrocardiograph and plasma BNP levels, and our data showed that the ejection fraction (EF) (Fig. 1e,f) and left ventricular fractional shortening (LVFS) (Fig. S1a) of diabetic rats showed a downward trend, while BNP levels gradually increased (Fig. 1g)
The Lactic dehydrogenase 1 (LDH1) and creatine kinase isoenzyme MB (CK-MB) activity as biomarkers in serum were evaluated cardiac injury, which was obviously increased in DCM, and was significantly inhibited treated with cyclovirobuxine D (CVB-D) (Fig. 1e–i)
Summary
Diabetic cardiomyopathy (DCM) is the principal cause of death in people with diabetes. Diabetic cardiomyopathy (DCM) is usually characterised by cardiac structure and functional disorders in individuals with diabetes independent of hypertension or ischemic coronary artery disease[1,2,3] It is the principal cause of death in patients with diabetes, no effective strategies currently exist to prevent the progression of DCM4. CVB-D protected against cardiac hypertrophy via the inhibition of the p38 pathways[25] It remains unclear if CVB-D could ameliorate oxidative stress via the activation of Nrf[2] signalling pathways and thereby prevent the cardiac pathologic structural damage and function disorder caused by diabetes. We investigate the beneficial effects and potential mechanism of CVB-D on DCM in vivo and in vitro
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