Abstract
Diabetic cardiomyopathy increases the risk of heart failure independent of coronary artery disease and hypertension. Phloretin (PHL) shows anti-inflammatory effects in macrophages. In this study, we explored the protective effects of PHL on high glucose (HG)-induced injury in diabetic cardiomyopathy in vivo and in vitro. Using streptozotocin-induced diabetic mouse model and incubating cardiac cells line under a HG environment, PHL were evaluated of the activities of anti-inflammation and anti-fibrosis. In the study, PHL treatment ameliorated cardiomyocyte inflammation injury, and reduced fibrosis in vivo and in vitro. PHL also improved cardiac biochemical criterions after 8 weeks of induction of diabetes in C57BL/6 mice. Molecular docking results indicated that silent information regulator 2 homolog 1 (SIRT1) bound to PHL directly and that SIRT1 expression was upregulated in the PHL-treated group in HG-induced H9C2 cells. Protective effect of PHL was been eliminated in silence SIRT1 H9C2 cells. Taken together, these results suggested that PHL suppressed HG-induced cardiomyocyte injury via restoring SIRT1 expression.
Highlights
It is widely accepted that diabetes mellitus poses a severe threat to human health [1]
Diabetic cardiomyopathy is a common complication of diabetes, usually causing patients decades of morbidity followed by severe outcomes, such as contractile dysfunction, concentric left ventricular hypertrophy, and dilated cardiomyopathy [1, 20]
The metabolic disturbances of diabetes are often accompanied by local inflammation and myocardial fibrosis that eventually develop into myocardial tissue damage and heart failure [26, 31, 32]
Summary
It is widely accepted that diabetes mellitus poses a severe threat to human health [1]. As one of the most frequently occurring vascular complications of diabetes, diabetic cardiomyopathy (DCM) exerts direct adverse effects on heart tissue. DCM can even result in heart failure [2]. The underlying pathophysiological mechanism involves abnormal activation in cardiomyocytes associated with abnormal cellular metabolism, chronic inflammation and fibrosis. These changes may lead to abnormalities in heart function and vascular dynamics [3]. The morbidity and mortality associated with these diseases mean that it is essential to develop drugs that can effectively delay myocardial remodeling and treat diabetic cardiac disease. The mechanism underlying in DCM has been increasingly recognized
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