中文摘要：

目的观察额尔敦-乌日勒对兔动脉粥样硬化易损斑块模型血清超敏C反应蛋白（high sensitivity C-reactive protein，hs—CRP）、单核细胞趋化蛋白-1（monocyte chemoattraetant protein-1，MCP-1）、细胞间粘附因子（intercellular adhesion molecule，ICAM-1）、血管粘附因子（vascular adhesion molecule-1，VCAM—1）的影响，以探讨额尔敦-乌日勒改善动脉粥样硬化易损斑块病变的可能机制。方法50只雄性新西兰大耳白兔随机分为4组，分别为正常组、模型组、额尔敦-乌日勒组及辛伐他汀组。通过高脂饲料、免疫损伤结合经股动脉球囊拉伤建立家兔动脉粥样硬化易损斑块模型，实验第8周开始给药至24周，取血检测炎症因子hs—CRP、MCP-1、ICAM-1和VCAM-1；取主动脉，光镜观察组织结构。结果额尔敦-乌日勒组主动脉病变程度相对较轻，纤维帽厚度与内中膜厚度比值高于模型组（P〈0．01），同时能明显降低动脉粥样硬化家兔血清hs—CRP、ICAM-1、VCAM-1、MCP-1含量（P〈0．01）。结论额尔敦-乌日勒可能通过抑制炎症反应，降低hs—CRP、ICAM-1、VCAM-1、MCP-1上升水平来发挥抗动脉粥样硬化（atherosclerosis，AS）的形成、发展和稳定易损斑块的作用。

英文摘要：

Objective To observe the influences of serum high sensitivity C-reactive protein （hs- CRP）, monoeyte chemoattractant protein-1 （MCP-1）, intercellular adhesion molecule （ICAM-1）, and vascular adhesion molecule-1 （ VCAM-1 ） on rabbit model of atherosclerotie vulnerable plaque with Eerdun- wurili and explore its possible mechanism. Methods Fifty New Zealand rabbits were randomly divided in- to 4 groups： the normal control group, the model group, the Eerdun-wurili group and the smivastatin group. The model was established by high fatty diet feeding, combined with immune injury and femoral arte- rial balloon tearing. From the 8th week the medication was given and the levels of serum hs-CRP, MCP-1, ICAM-1 and VCAM-1 were measured at the 24th week of experiment. Tissue structure of aortic were ob- served under light microscope. Results Aortic lesions is relatively milder in the Eerdun-wurili group and the fibrous cap thickness and lntima media thickness ratios in the Eerdun-wurili group were higher than those of model group; besides, the levels of serum hs-CRP, ,ICAM-1, ,VCAM-I,and MCP-1 were de- creased significantly （ P 〈 0.01 ）. Conclusion Eerdun-wurili could prevent AS formation and stabilize atheroselerosis vulnerable plaque. It acts by suppressing the inflammation reaction.