[Influence of daidzein on left ventricular remodeling in rats with hypertrophic myocardium induced by pressure overload].
Li Zhou, Qing Zhou, Xiao‐Qing Xiong, Jian-xin Liu, Wei He
Abstract
Li Zhou, Qing Zhou, Xiao‐Qing Xiong, Jian-xin Liu, Wei He
Abstract
OBJECTIVE: To investigate the protective effects of daidzein (DD) on ventricular remodeling in rats with myocardial hypertrophy induced by pressure overload and its mechanism. METHOD: Myocardial hypertrophy 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, 120 mg kg(-1)). 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 dyeing by HE colar were measured. The hydroxyroline, nitric oxide (NO) and the activity of nitric oxide synthetase (NOS) and Na+ -K+ -ATPase, Ca2+ -ATPase in left ventricle were quantified with spectrophotometry and the angiotension II (Ang II) in left ventricle and serum was messured with radioimmunoassay. RESULT: After treatment of the left ventricular with DD, vs aorta-contricted model group, NO content, cNOS and Na+ -K+ -ATPase, Ca2+ -ATPase activity were significantly increased, the content of AngII in left ventricle and serum and iNOS activity and the ratio of HW/BW, LVI, MD were significantly reduced. CONCLUSION: DD has protective effects on ventricular remodeling in rats with myocardial hypertrophy induced by pressure overload and its mechanism may be related to raising NO content and reducing the level of Ang II.
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OBJECTIVE: To investigate the protective effects of daidzein (DD) on ventricular remodeling in rats with myocardial hypertrophy induced by pressure overload and its mechanism. METHOD: Myocardial hypertrophy 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, 120 mg kg(-1)). 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 dyeing by HE colar were measured. The hydroxyroline, nitric oxide (NO) and the activity of nitric oxide synthetase (NOS) and Na+ -K+ -ATPase, Ca2+ -ATPase in left ventricle were quantified with spectrophotometry and the angiotension II (Ang II) in left ventricle and serum was messured with radioimmunoassay. RESULT: After treatment of the left ventricular with DD, vs aorta-contricted model group, NO content, cNOS and Na+ -K+ -ATPase, Ca2+ -ATPase activity were significantly increased, the content of AngII in left ventricle and serum and iNOS activity and the ratio of HW/BW, LVI, MD were significantly reduced. CONCLUSION: DD has protective effects on ventricular remodeling in rats with myocardial hypertrophy induced by pressure overload and its mechanism may be related to raising NO content and reducing the level of Ang II.
Key concepts: Ventricle, Internal medicine, Pressure overload, Chemistry, Endocrinology, Muscle hypertrophy, Nitric oxide, Left ventricular hypertrophy