炎症控制下内膜新生血管在动脉硬化发生发展中的作用

目的:研究在控制炎症水平的情况下内膜新生血管在动脉硬化发生、发展中所起到的具体作用。方法:高脂饮食8周造成大鼠动脉硬化模型,使用阿司匹林抑制动脉硬化大鼠的基础炎症水平,分别给予内皮抑素和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、CD31表达量。结果:模型组血脂水平与空白对照组有显著差异(P<0.05);硬化动脉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/中膜面积比值(I A/MA)差异无显著性(P>0.05),但低于单纯模型对照组(P<0.05)。结论:仅仅依靠内膜新生血管的数量还不能够完全作为评价动脉硬化发生发展的标准,内膜新生血管的数量可能仅是炎症水平的一种外部表现形式。

Role of Intimal Neovascularization in Angiosclerosis Under the Control of Inflammation

Objective: To investigate the role of intimal neovascularization in atheromatous plaque under the control of inflammation. Method: 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 the expression of CD31. Results: The serum cholesterol level were similar in model group (P >0.05), higher than blank comparison(P <0.05) ; the amount of intimal neovascularization: group VEGF_ 165 >group model control group>group aspirin>group endostatin > group blank group(P <0.05). Conclusion: The amount of intimal neovascularization is not the criterion to evaluate the development of angiosclerosis. It’s just the reflection of inflammation.