粥样斑块发生发展过程中炎症和新生内膜血管之间的关系

目的为研究在控制炎症水平的情况下内膜新生血管在动脉粥样斑块发生、发展中所起到的具体作用。方法高脂饮食8周造成大鼠动脉粥样硬化（AS）模型,然后使用阿司匹林抑制AS大鼠的基础炎症水平,分别给予内皮抑素和血管内皮生长因子165（VEGF165）两种不同方法处理大鼠,8周后比较血脂、胸主动脉形态学、以及检测CD31表达水平以计算内膜新生血管的数量。结果模型组的血脂水平高于空白对照组（P<0.05）;粥样斑块内部的新生血管数量VEGF165+阿司匹林组>单纯模型对照组>阿司匹林组>内皮抑素+阿司匹林组>空白对照组（P<0.05）;阿司匹林组、内皮抑素+阿司匹林组和VEGF165+阿司匹林组的内膜面积/中膜面积的比值（IA/MA）差异无显著性,但高于单纯模型对照组（P<0.05）。结论在用阿司匹林抑制AS模型大鼠基础炎症的情况下,VEGF165和内皮抑素对血管内膜生成的影响无显著差异。

Relation between inflammation and intimal neovascularization in the progress of atheromatous plaque

AIM To investigate the role of intimal neovascularization in atheromatous plaque under the control of inflammation.METHODS To establish the model of Atherosclerosis,employing asprin to control basic inflammation level.The rats were treated with endostatin and VEGF_(165) separately.8 weeks later,compared the serum cholesterol,morphology of aorta and count the amount of intimal neovascularization by measure the expression of CD31.RESULTS The serum cholesterol level of model group was higher than blank comparison(P<0.05);the amount of intimal neovascularization: VEGF_(165)group> model control group>aspirin group> endostatin group> blank comparison group(P<0.05);the IA/MA ratio was no different in all groups(P<0.05).CONCLUSION when asprin was used to control the inflammation of AS model of rats,the VEGF_(165) and endostatin had no significant effect on the intima.