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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
OBJECTIVE: To establish an animal model of atherosclerosis (AS) and to explore the molecular mechanisms that affect the formation and development of AS. Methods: Ten rabbits were fed with high-fat diet for one week. The carotid artery was used retrograde approach. The balloon catheter was inserted into the iliac artery and randomly placed into the distal part of the iliac artery to damage the intima. One side is not damaged, as a control), the iliac artery stenosis model was established 6 weeks after hyperlipidemic feeding and confirmed by imaging, pathological light microscopy, electron microscopy and immunohistochemical analysis, and nuclear factor κappaB (NF κB), and insulin like growth factor 1 (IGF 1) by immunohistochemistry. Results: In the model group, the average stenosis of arterial angiography was 69 0 ± 19 12%. HE staining showed that the intima was thickened to eccentric luminal stenosis. The thickening intima mainly consisted of foam cells and smooth muscle cells, The membrane and smooth muscle cells migrated into the intima. The ultrastructural changes of NF-κB and IGF-1 were observed by electron microscopy. The expression of NF-κB and IGF-1 was higher than that of the control group (p <0.05 or p < 0 0 0 5). Conclusions: (1) Rabbit iliac artery stenosis model was established successfully by balloon injury of intima and hyperlipidemic diet, most of which were eccentric and limited 40% ~ 100% stenosis. The model was accurate and reliable (2) The activation of NF-kappa B and its target gene IGF-1 is closely related to the occurrence and development of AS lesion