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小剂量Aspirin对动脉粥样硬化兔主动脉斑块炎症反应和COX-2表达的影响 被引量:1

Effects of Low-dose Aspirin on Expression of COX-2 and Inflammation Process in Aorta Lesions of Atherosclerotic Rabbit
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摘要 目的探讨小剂量阿司匹林对兔动脉粥样硬化主动脉斑块炎性过程和COX-2表达的影响。方法24只雄性新西兰兔随机分为对照组(喂食普通兔料)、高脂模型组(喂食高脂饲料)、阿司匹林组(喂食高脂饲料并给与小剂量阿司匹林干预),饲养12周后处死动物,取主动脉进行病理学检查,测定斑块面积,采用免疫组化方法观察各组巨噬细胞的表达情况,Western-bolt分析COX-2的表达。结果病理学大体观察发现,对照组、高脂模型组和阿司匹林组主动脉壁脂质斑块面积占整条主动脉内壁面积的百分比分别为0%、(59.62±10.74)%、(48.33±7.85)%,各组间两两比较均有显著性差异(P<0.05)。阿司匹林组斑块区巨噬细胞含量、COX-2表达明显低于高脂模型组。结论小剂量阿司匹林干预可以通过抑制病灶区的炎症反应、COX-2的表达来有效减轻高脂饮食所致的新西兰兔动脉粥样硬化的严重程度。 Objective To examine the effects of low- dose aspirin on atherosclerotic lesions and the expression of COX - 2 in rabbits fed with cholesterol - enriched diet. Methods Twenty - four male New Zealand white rabbits were randomly divided into standard rabbit chow group, cholesterol diet group, and cholesterol diet associated with low- dose aspirin group. The rabbits were sacrificed after 12 wk. The aorta was harvested for pathologic morphology observation, and the expressions of macrophage and COX - 2 were analyzed by immunohistochemistry method and western - blot. Results The aortic plaque / intima size was 0 %, .59.62 ± 10.74 % and 48.33 _± 7.8.5 % in the control group, the cholesterol - fed alone group, nd low- dose aspirin treated group respectively under morphology observation (P〈 0.05). The expression of macrophage in low - dose aspirin treated group was decreased as compared with that in the untreated cholesterol fed alone group. The expression of COX - 2 in atherosclerotic lesions of low dose aspirin treated group was significantly decreased as compared with that of the untreated cholesterol fed alone group. Conclusions Low- dose aspirin can suppress the pro- gression of experimental atherosclerosis. The expressions of COX - 2 and macrophage in lesions are found to be decreased after low - dose aspirin treatment in experimental atherosclerotic rabbits.
出处 《实用预防医学》 CAS 2007年第6期1712-1715,共4页 Practical Preventive Medicine
关键词 阿司匹林 动脉粥样硬化 环氧合酶2 Aspirin Atherosclerosis COX-2
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