中文摘要：

目的 观察阿托伐他汀对载脂蛋白E基因缺陷（apoE-／-）小鼠实验性动脉粥样硬化（AS）病变形成及血管细胞黏附分子-1（VCAM-1）表达的影响，探讨阿托伐他汀抑制AS病变形成的可能机制。方法 将apoE-／-小鼠随机分为3组：阿托伐他汀高、低剂量组、模型组（等量生理盐水），每组8只，给药第8周后全部处死。酶法检测血清脂质含量；比色法检测氧化指标一氧化氮（NO）、总抗氧化能力（TAC）及丙二醛（MDA）；病理图像分析法测定主动脉AS斑块面积及其与管腔面积的比值；免疫组织化学染色方法测定主动脉壁VCAM-1表达。结果 阿托伐他汀高、低剂量组与模型组apoE-／-小鼠比较显示：（1）阿托伐他汀（高、低剂量）可以显著降低总胆固醇、甘油三酯水平（P〈0．01），升高高密度脂蛋白胆固醇水平（P〈0．01）；（2）明显增加血浆NO及TAC（P〈0．01），减少MDA的生成（P〈0．01）；（3）阿托伐他汀可减少斑块面积与管腔面积比值（P〈0．01）；（4）阿托伐他汀可下调VCAM．1的表达（P〈0．01）。结论 阿托伐他汀可能通过调节apoE-／-小鼠血脂代谢、增强其抗氧化能力及下调主动脉壁VCAM-1表达，抑制apoE-／-小鼠As病变形成的发展。

英文摘要：

Objective To study the effect of atorvastatin on the atherosclerotic（AS） lesion formation and expression of vascular cell adhesion molecule-1 （VCAM-1） and the mechanism of inhibitory effect of atorvastatin on the AS lesion formation in apoE-deficienct （apoE-/-）mice.Methods Thirty-two male apoE-deficienct mice were randomized into three groups： atorvastatin high dose group, low dose group and control group. At the end of eight weeks of drug administration, all mice were sacrificed. The serum levels of total cholesterol, triglyceride and high-density lipoprotein-cholesterol were measured by enzyme method. Light microscopy was adopted to assess the degree of atherosclerotic plaque of aortic wall and pathological picture analysis was performed to calculate the ratio of area of aortic AS plaque to area of vessel lumen. The expression of VCAM-1 was studied by immunohistochemistry. Results As compared with the control group, atorvastatin could reduce the levels of serum TC ,TG significantly（ P〈0.01）, and elevate HDL-C level significantly（ P〈0.01）.It could increase the levels of serum NO and total anti-oxidation capacity significantly（ P〈0.01）, but reduce the level of serum MDA significantly（ P〈0.01 ）. It could also reduce the extent of atherosclerotic plaque of aorta significantly （ P 〈 0.01） and down-regulate the expression of VCAM-1 in aortic wall. Conclusion Atorvastatin could inhibit the occurrence and development of atherosclerotic lesions by regulating lipid metabolism, enhanc ing anti-oxidation abihty and down-regulating expression of VCAM-1 in aortic wall in apoE-/- mice.