Rosuvastatin dose-dependently reduced myocardial collagen volume fraction and inhibited TGF-β1 expression, alleviating myocardial fibrosis in a rat model of diabetic cardiomyopathy.
Does rosuvastatin reduce TGF-β1 expression and myocardial fibrosis in a rat model of diabetic cardiomyopathy?
In a rat model of diabetic cardiomyopathy, rosuvastatin attenuated myocardial fibrosis and ventricular remodeling, likely by inhibiting TGF-β1 expression.
Absolute Event Rate: 7.29% vs 12.31%
p-value: p=<0.05
This study aimed to investigate the effects of rosuvastatin on TGF-β1 expression, cardiac fibrosis, ventricular remodeling and cardiac function in diabetic cardiomyopathy rats. Twenty-seven diabetic rats induced by streptozotocin intraperitoneal injection were randomly divided into three groups, viz. diabetic, rosuvastatin low-dose (Ros-L) and high dose group (Ros-H). Intervention group were given rosuvastatin 2 mg/kg/d and 5 mg/kg/d orally, respectively. After 10 weeks, the levels of glycosylated hemoglobin (HbA1c), creatine phosphokinase isoenzyme (CK-MB), plasma brain natriuretic peptide (BNP), myocardial collagen volume fraction (CVF) and left ventricular mass index (LVWI) were measured. CK-MB levels in Ros-H and Ros-L rats were lower than in the diabetic group. Rosuvastatin alleviated myofibrosis cordis and fibroplastic proliferation. LVWI, BNP, CVF and TGF-β1 mRNA and protein levels in the diabetic group were higher than in the control, but were reduced after rosuvastatin treatment. These results demonstrate that rosuvastatin dose-dependently reduces TGF-β1 expression and inhibits the development of myocardial fibrosis in diabetic cardiomyopathy.
Ma et al. (2013) studied Diabetic cardiomyopathy (n=37). Rosuvastatin vs. Untreated diabetic rats was evaluated on Myocardial collagen volume fraction (CVF) (p=<0.05). Rosuvastatin dose-dependently reduced myocardial collagen volume fraction and inhibited TGF-β1 expression, alleviating myocardial fibrosis in a rat model of diabetic cardiomyopathy.