补阳还五汤抗家兔动脉粥样硬化形成及机制
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国家自然科学基金 (C3 960 0 197);国家教育部优秀青年教师基金 (教人司 2 0 0 1:3 9号 )


"Buyang Huanwu Decoction" Inhibited Pathogentic Process of Atherosclerosis Induced by Cholesrol-rich Diet and Its Mechanism in Rabbits
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    摘要:

    为了观察补阳还五汤抗动脉粥样硬化的作用及机制,给予家兔高脂饮食和补阳还五汤,用组织学方法观察动脉壁病理形态学改变,并测定血清中总胆固醇、甘油三酯、内皮素、一氧化氮及FⅦ促凝活性水平。结果显示,与高脂组相比,补阳还五汤组血清总胆固醇和甘油三酯明显降低(P<0.01);血浆FⅦ促凝活性和一氧化氮水平明显降低(P<0.01);主动脉、腹主动脉和冠状动脉粥样斑块面积显著减少(P<0.01)。提示补阳还五汤具有抗动脉粥样硬化形成的作用,其机制可能与降低血脂和FⅦ促凝活性有关

    Abstract:

    Aim To determine whether the extract of Buyang huanwu decoction(BHD)inhibit the pathogenetic progress of atherosclerosis induced by cholesrol rich diet and to elucidate its mechanism in rabbits. Methods Three groups of rabbits received the following different diets for 9 weeks: ordinary diet(OD) group, model of atherosclerosis (MA) group(ordinary diet plus 1% cholesterol and 3.3% fat), and MA plus BHD [5 g/(kg·d)] group. Plasma lipids, endothelin 1(ET 1), nitric oxide(NO) and factor Ⅶ procoagulant activity(FⅦ:C) were detected and the histological atherosclerotic changes in aortic, abdominal aortic and coronary artery were evaluated. Results Compared with the MA group, serum total cholesterol(12.70±6.17 vs 26.6±10.41 mmol/L, p<0.01), triglycerides (1.05±0.25 vs 2.72±1.55 mmol/L, p<0.01), FⅦ:C(135.36±34.54 vs 287.84±66.87, p<0.01), and NO (30.23±12.91 vs 112.30±23.00, p<0.01) were significantly lower in the MA plus BHD group, and this decoction inhibited theprogression of aortic, abdominal aortic and coronary intimal plaques and reducedaortic intimal thickening. Conclusions These datas suggested that BHD have antiatherogenic effects and its mechanism might associate with the decrease of plasma cholesterol, triglycerides, nitric oxide and factor Ⅶ procoagulant activity. (① A kind of traditional Chinese decoction consisted of seven kinds of Chinese medicine: astragalus; angelica; ligusticum; paeonia; earthworm; swietenia and carthamus.)

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尚改萍,文志斌,何晓凡,汉建忠,李俊成,贺石林.补阳还五汤抗家兔动脉粥样硬化形成及机制[J].中国动脉硬化杂志,2002,10(2):112~114.

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  • 收稿日期:2001-10-08
  • 最后修改日期:2002-02-24
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