Protection of daidzein on myocardial hypertrophy and fibrosis in rats

Objective To investigate the protective effects of daidzein (DD) on myocardial hypertrophy and fibrosis induced by pressure overload in rats and to study its mechanism. MethodsMyocardial hypertrophy and fibrosis model of rats induced by pressure overload was prepared by constricting abdominal aorta. The operated rats were randomly divided into sham operated control group, aorta-constricted model group, and three DD groups (30, 60, and 120 mg/kg). Four weeks later, the heart-weight (HW), left ventricular weight (LVW), the ratio of HW/BW and LVW/BW (LVI), and the cardio-myocyte diameters (MD) after dying by HE color were measured. The content of collagen and nitric oxide (NO), the activity of calcineurin (CaN) and Na+, K+-ATPase, Ca2+-ATPase in the left ventricle were quantified with spectrophotometry. The angiotension Ⅱ (AngⅡ) in the left ventricle was messured with radioimmunoassay. Results In aorta-constricted model group, the ratio of HW/BW, LVI, and MD as well as the content of collagen and AngⅡ, the activity of CaN in the left ventricle was significantly increased, and Na+, K+-ATPase, Ca2+-ATPase activity and NO content in the left ventricle were obviously decreased. After treatment of the left ventricular with DD, NO content, Na+, K+-ATPase, Ca2+-ATPase activity were significantly increased, the content of collagen and of AngⅡ and the activity of CaN in the left ventricle and the ratio of HW/BW, LVI, and MD were significantly reduced. ConclusionDD has protective effects on ventricular remodeling in rats with myocardial hypertrophy and fibrosis induced by pressure overload and its mechanism may be related to raising NO content and reducing the level of AngⅡ and the activity of CaN.