【摘要】 目的 :建立动脉粥样硬化狭窄 (Atherosclerosis,AS)动物模型并探讨影响AS形成、发展的分子生物学方面的机制。方法 :10只大耳白兔 ,高脂饲料喂饲一周后 ,采用颈动脉为逆行入径 ,将球囊导管顺行插入并随机至一侧髂动脉远端 ,使其内膜损伤 ,(另一侧不损伤 ,作为对照 ) ,高脂喂养 6周后建立髂动脉AS狭窄模型 ,并通过影像学、病理学光镜、电镜及免疫组化分析证实 ,并观察核因子 κB(nuclearfactor κappaB ,NF κB)、胰岛素样生长因子 1(insulin likegrowthfactor 1,IGF 1)的免疫组织化学分析。结果 :模型组动脉造影显示平均狭窄度 6 9 0± 19 12 % ;HE染色示内膜明显增厚至管腔偏心性狭窄 ,增厚内膜主要由泡沫细胞、平滑肌细胞组成 ,内弹力膜分离断裂 ,中膜平滑肌细胞迁移入内膜层 ;电镜示膜结构损伤 ,可见凋亡小体 ;免疫组化示NF κB、IGF 1蛋白表达量均高于对照组 (p <0 0 5或p <0 0 0 5 )。结论 :(1)通过球囊损伤血管内膜加高脂饮食成功建立了兔髂动脉AS狭窄模型 ,多数为偏心、局限性的 4 0 %～ 10 0 %的狭窄 ,模型确切、可靠、是用于经皮冠状动脉腔内成形术 (per cutaneoustransluminalcoronaryangioplasty ,PTCA)的理想动物模型 ;(2 )NF κB及其靶基因IGF 1的激活与AS病变的发生与发展密切相关更多还原

【Abstract】 Objective:To set up atheroscl erotic stenosis (AS) animal model and study the mechanism of affecting AS form and development in molecule biology.Methods:With carotid converse path,ballon catheter was sequential inserted into the distal of one side iliac artery randomly and damaged the intima(the other side was not injured,as control)in 10 cholesterol-fed rabbit.After 6 weeks of fat-rich feeding,the iliac artery AS model was set up,which was confirmed by using angiography?pathologic light microscope?electron microsope and immunohistochemistry.Results:angiography:the average luminal diameter stenosis was 69.0%±19.12%;HE:intima thickened to make the cavity obvious stenosis,the thicking of intima was mainly composed of abundant foam cells and smooth muscle cells,internal elastic membrance was ruptured;EM:membrane structure was damaged,apoptic body(apoptosome)can be seen;IMHC:nuclear factor-κ B(NF-κ B)and insulin-like growth factor 1(IGF-1)protein expressed significantly higher than control group(P<0.05 or P<0.005).Conclusious:AS model is successfully set up by ballon catheter endothelial injury of iliac artery in cholesterol-fed rabbit,which is the perfect animal model for percutaneous transluminal coronary angioplasty(PTCA);the activation of NF-κB and its target gene IGF-1 nearly relate to the form and development in AS.更多还原