Why the study?
Oxidative stress contributes critically to diabetic cardiomyopathy, and forskolin reduces oxidative stress, prompting investigation into its effects and molecular mechanisms in diabetic hearts.
Does forskolin improve cardiac diastolic function and reduce cardiac fibrosis in mice with streptozotocin-induced diabetic cardiomyopathy?
Does forskolin improve cardiac diastolic function and reduce cardiac fibrosis in mice with streptozotocin-induced diabetic cardiomyopathy?
Forskolin demonstrates cardioprotective effects in a mouse model of diabetic cardiomyopathy by improving diastolic function and reducing oxidative stress and fibrosis.
FSK attenuates DCM via reduced oxidative stress and fibrosis in mice; leaves open clinical translation pending human trials.
Background . Diabetic cardiomyopathy is one of the cardiac complications in diabetes patients, eventually resulting in heart failure and increasing morbidity and mortality. Oxidative stress is a critical pathological feature in diabetic hearts, contributing to the development of DCM. Forskolin (FSK) was shown to reduce oxidative stress. This study was aimed at investigating the effects of FSK on diabetic hearts and the relevant molecular mechanisms. Methods . Streptozotocin‐ (STZ‐) induced diabetes in mice was treated with FSK through intraperitoneal injection. Cardiac functions were evaluated by echocardiography. Hematoxylin‐eosin and Masson trichrome staining was employed to determine heart morphological changes and cardiac fibrosis, respectively. Cardiac fibrosis‐related markers were detected by western blot. Superoxide dismutase activity, reduced/oxidized glutathione ratio, and malondialdehyde concentration in left ventricles were determined using respective commercial kits. Results . Abnormal cardiac diastolic dysfunction and cardiac fibrosis were observed in diabetic hearts. FSK treatment significantly improved the cardiac diastolic function and attenuated the abnormal morphological change in diabetic hearts. Moreover, FSK treatment in diabetic mice decreased the expression of fibronectin, collagen I, TGF‐ β , and α ‐SMA and reduced myocardial fibrosis. Furthermore, we observed that FSK significantly blocked oxidative stress in diabetic hearts. Conclusions . Our study demonstrates that FSK protects against the development of DCM in STZ‐induced diabetes in mice. Our study suggests that FSK might be a potential target for drug development in treating DCM.
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Zhang et al. (2021) studied this question.
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