绞股蓝总皂甙对兔实验性动脉粥样硬化斑块形成的影响

Effect of Gypenosides on Formation of Atherosclerotic Plaque of Aorta in Hypercholesterolemic Rabbits

为了探讨绞股蓝总皂甙防止动脉粥样硬化的作用及其机制．在新西兰兔食饵性动脉粥样硬化模型上，观察了绞股蓝总皂甙治疗性给药对主动脉壁粥样硬化斑块形成及脂质过氧化的影响。发现绞股蓝总皂甙（120mg／d）治疗四周能减少主动脉壁斑块形成．苏丹IV染色及形态计量学分析显示绞股蓝总皂甙治疗组的斑块面积较之高脂组减少了37％；主动脉壁脂质过氧化程度也明显减轻，丙二醛含量仅为高脂组的67％。此外，还观察到绞股蓝总皂甙在减少主动脉壁斑块形成和脂质过氧化的同时，还能保护血管壁释放或合成一氧化氮的能力，并防止因长期高胆固醇血症引起的主动脉壁Ca2+超载。绞股蓝总皂甙的作用与抗氧化剂维生素E相似。

Aim To investigate the effects and mechanisms of Gypenosides on the atherosclerotic plaque formation in rabbit with hypercholesterolemia.Methods 23 male New Zealand white rabbits were assigned to four groups:5 rabbits in control group were fed with a normal diet;8 rabbits in hyperc-holesterolemic group were fed with 1% cholesterol diet for 9 weeks;In gypenosides and vitamine E (Vit E)treat groups,5 weeks after fed with 1% cholesterol di-et the animals were fed with 1% cholesterol diet con-taining gypenosides or Vit E for another 4 Weeks.Sudan IV stain was used to show the relative area ofatherosclerotic plaque.Lipid peroxides of aorta were estimated by the thiobarbituric acid method.Nitrite,the matabolic product of nitric oxide,was determined according to a modified Griess' method.The Ca2+.K+ and Na+ content of aorta were measured in means of atom absorption.Results Gypenosides treatment (120 mg/d,4weeks)inhibited formation of atherosclerotic plaque as shown by 37% reduction of plaque areas comparing to 1% cholesterol treatment along.Gypenosides also decreased lipoperoxidation of aorta by 33%.In addi-tion,gypenosides protected nitric oxide release of aorta against hypercholesterolemia damage and reduced Ca2+content of aorta by 50%.However,both hyperc-holesterolemia and gypenosides had no influence on K+and Na+ content of aorta.Vit E showed the same ef-fect as gypenosides did.Conclusion Gypenosides atlenuates the formatiom of atherosclerotic plague and lipoperoxidation of aorta induced by hypercholesterolemin in rabbit.The mecha-nisms of antiatherogenic effects of gypenosides might include its protection on nitric oxide and its inhibition on calcium overload.