芪参降脂饮预防动脉粥样硬化发生的可能机制

目的:探讨芪参降脂饮防治动脉粥样硬化发生的作用机制。方法:24只SD大鼠随机分为3组:对照组8只,喂以普通饲料;模型组8只,喂以高脂饲料;中药组8只,喂以高脂饲料,同时给以芪参降脂饮灌胃。8周后急性处死大鼠。取血测血脂、血清丙二醛水平及超氧化物歧化酶活性;用免疫组化和Westernblot检测主动脉壁细胞间黏附分子1(ICAM1)蛋白表达水平。苏木素伊红染色观察主动脉组织形态学变化。结果:中药组主动脉内皮损伤明显轻于模型组,中膜平滑肌排列亦较模型组整齐。中药组血脂和丙二醛水平明显低于模型组(P<0.01),而超氧化物歧化酶活性则明显高于模型组(P<0.05)。模型组大鼠主动脉壁ICAM1蛋白表达量明显高于中药组(P<0.01)。结论:芪参降脂饮能够抑制实验大鼠动脉粥样硬化的发生发展,其作用可能是通过降低血脂,清除氧自由基来保护血管内皮免受损伤,同时下调ICAM1在主动脉壁的表达来实现的。

Functions of Qishenjiangzhiyin in Obviating Atherosclerosis and Its'''' Possible Mechanism

Objective:To study the mechanism of Qishenjiangzhiyin in obviating atherosclerosis. Methods:Twenty-four male SD rats were randomly equally divided into three groups:control group,model group and treatment group. Rats in control group were fed with normal diet. Rats in model group were fed with high cholesterol diet. Rats in treatment group were fed with high cholesterol diet plus Qishenjiangzhiyin. Eight weeks later, all the rats were killed. Blood-fat level,serum malondialdehyde(MDA) concentrations and superoxide dismutase(SOD) activity were measured. The aortas were collected for histomorph-ology studies. The intercellular adhesion molecule-1(ICAM-1) expression of aorta was measured by immunohistochemistry and Western blot. Results: The endothelial damage of the aortas in treatment group was less severe than that in model group. The smooth muscle cells of the aortas in treatment group lined up in an order better than those in model group. The level of blood-fat and serum MDA decreased significantly as compared with those of model group (p<0.01).Serum SOD activity increased in treatment group as compared with those of model group(p<0.05). ICAM-1 expression level of aortas in treatment group was significantly lower than those in model group (p<0.01). Conclusion: Qishenjiangzhiyin can restrain the occurrence and development of artherosclerosis .The possible mechanism may be associated with the protection of blood vessel endothelium from being damaged through reducing blood-fat and eliminating oxygen-derived free radicals ,and down-regulation of expression of ICAM-1 in aorta.