摘要
目的研究大豆异黄酮(daidzein,DD)对大鼠压力负荷性心肌肥厚及纤维化的保护作用及其机制。方法采用腹主动脉缩窄法制备大鼠心肌肥厚模型。大鼠随机分为假手术组、模型组、DD(30、60、120mg/kg)组;4周后处死大鼠,测量大鼠全心质量指数(HW/BW)和左心室质量指数(LVW/BW,即LVI),测定心肌纤维直径(MD);分别检测心肌组织中胶原水平、血管紧张素(Ang)、一氧化氮(NO)的量和钙调神经磷酸酶(CaN)、Na+,K+-ATP酶、Ca2+-ATP酶活性。结果模型组大鼠的HW/BW、LVI、MD明显增大;心肌组织CaN活性、胶原水平及Ang的量明显增高;NO水平和Na+,K+-ATP酶、Ca2+-ATP酶活性显著降低。与模型组比较DD能显著提高心肌组织NO量和Na+,K+-ATP酶、Ca2+-ATP酶活性,降低CaN活性;明显抑制心肌组织Ang和胶原的产生;减轻心脏质量参数(HW/BW、LVI)及MD,抑制心肌肥厚及纤维化。结论DD对腹主动脉缩窄所致大鼠心肌肥厚及纤维化有保护作用,可能与其升高NO量、降低CaN活性、抑制Ang产生有关。
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. Methods Myocardial 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, Ca^2＋-ATPase in the left ventricle were quantified with spectrophotometry. The angiotension Ⅱ （Ang K ） 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 Ang Ⅱ , the activity of CaN in the left ventricle was significantly increased, and Na^＋, K^＋-ATPase, Ca^2＋-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, Ca^2＋-ATPase activity were significantly increased, the content of collagen and of Ang Ⅱ and the activity of CaN in the left ventricle and the ratio of HW/BW, LVI, and MD were significantly reduced. Conclusion DD 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 Ang Ⅱ and the activity of CaN.
出处
《中草药》
CAS
CSCD
北大核心
2007年第11期1673-1676,共4页
Chinese Traditional and Herbal Drugs
基金
江西省卫生厅中医药管理处资助项目(2006A66)
