中文摘要：

目的探讨血管内皮细胞损伤和血清内源性代谢物的变化与动脉硬化闭塞症（ASO）发病的关系。方法采用高脂饮食饲喂及动脉内膜损伤的方法制作大鼠ASO模型，造模后8周用光镜观察动脉大体形态，Percoll密度梯度离心法测定外周血中循环内皮细胞（CEC）数量，酶联免疫吸附双抗体夹心法检测血清内皮素1（ET-1）和一氧化氮（NO）水平，基于气相色谱一质谱联用技术（GC／MS）的代谢组学方法分析血清中内源性代谢物的变化。结果成功建立了大鼠ASO模型，ASO大鼠外周血中CEC数量明显增多，血清ET-1水平均较正常对照明显升高，NO水平较正常对照明显降低（P〈0．01）；与正常对照相比，ASO大鼠血清中的糖类、氨基酸类、脂肪酸类物质的代谢水平均发生了明显的改变。结论血管内皮细胞损伤和血清内源性代谢物的变化介导了ASO的发生，保护血管内皮的功能、调节内源性代谢物的平衡应是ASO的重要治疗靶点。

英文摘要：

Ahn To discuss the relationship between vascular endothelial cell injury, changes of serum endoge- nous metabolites and pathogenesis of arteriosclerosis obliterans （ASO）. Methods ASO models were constructed with the method of high-fat diet plus intimal injury. At 8 weeks after operation, the arterial morphology was observed using light microscopy, the number of circulating endothelial cells （CEC） was determined using percoll density gradient centrifu- gation method, serum endothelin-1 （ET-1） and nitric oxide （NO） levels were detected using ELISA double antibody sand- wich assay, changes of endogenous metabolites in serum were analyzed with the metabonomics method-based gas chromatog- raphy-mass spectrometry （GC/MS） technology. Results Rat models of ASO were established successfully, the num- ber of CEC in ASO rat peripheral blood increased significantly, the serum ET-1 level was significantly higher, and the level of NO was significantly less than normal control rats after operation （P 〈 0. 01 ）. Compared to normal control group, me- tabolism of the sugars, amino acids, fatty acids in serum of ASO rats were significantly changed. Conclusions Vas- cular endothelial cell injury and changes of serum endogenous metabolites mediated ASO, protecting the vascular endotheli- al function and adjusting the balance of the endogenous metabolites should be important therapeutic targets of ASO.