通过本室已建立的人清道夫受体AI转基因小鼠对动脉粥样硬化的易感性的研究 ,以阐明人清道夫受体在动脉粥样硬化中的作用。为此 ,用人清道夫受体转基因小鼠 (F3)的纯合子 (TghSR AI+ +)、杂合子 (TghSR AI+ )、聚合酶链反应阴性 (TghSR AI )和C57BL 6小鼠各 1 2只 ,喂高脂高胆固醇饲料 1 4周后 ,取动物心脏和主动脉 ,作连续石蜡切片或冰冻切片 ,HE染色或油红O染色 ,用图象分析系统测量和计算主动脉动脉粥样硬化病变面积。结果发现 ,喂高脂高胆固醇饲料 1 4周后 ,小鼠动脉粥样硬化病变主要位于主动脉窦至主动脉弓的区域内 ,但纯合子鼠的动脉粥样硬化病变除在整个主动脉根部外 ,病变已扩展到胸主动脉、冠状动脉和肾动脉。C57BL 6鼠和阴性小鼠的主动脉窦区瓣膜附着处仅有轻微损伤。计算机图象分析发现 ,纯合子鼠主动脉粥样硬化病变的平均面积为 1 4 4 864± 1 71 0 3μm2 ,与杂合子组 (1 1 1 32 2± 1 0 71 3μm2 )相比 ,差异有显著性统计学意义 (P <0 .0 5) ;与聚合酶链反应阴性 ( )小鼠或C57BL 6小鼠相比 ,差异有非常显著性统计学意义 (P <0 .0 1 )。提示纯合子鼠动脉粥样硬化病变最严重 ,其次是杂合子鼠 ,而非转基因小鼠主动脉动脉粥样硬化病变较轻。转基因小鼠肝、肾也可见明显的病变。此结果提示 Through this room has been established scavenger receptor AI transgenic mice atherosclerosis susceptibility study to elucidate the role of human scavenger receptor in atherosclerosis. For this purpose, 12 homozygotes (TghSR AI +), heterozygotes (TghSR AI +), PCR-negative (TghSR AI) and C57BL 6 mice were screened for the scavenger receptor-transgenic mice (F3) After 4 weeks of high-fat and high-cholesterol diet, the heart and aorta were taken for serial paraffin sections or frozen section, stained with HE or Oil Red O, and the area of ​​aortic atherosclerosis was measured and calculated by image analysis system. The results showed that atherosclerosis lesions in mice were mainly located in the aorta to aorta arch after feeding with high-fat and high-cholesterol diet for 14 weeks. However, in atherosclerosis lesions of homozygous rats except for the entire aortic root, Lesions have been extended to the thoracic aorta, coronary and renal arteries. C57BL 6 mice and negative mice showed only slight damage to the aortic sinus valve attachment. Computer image analysis showed that the average area of ​​aortic atherosclerosis in homozygous mice was 144.4864 ± 1.71.0 3μm2, which was significantly lower than that in the heterozygous group (11 1 32 2 ± 1 0 71 3μm2) Significant statistical significance (P <0. 05); Compared with the polymerase chain reaction negative () mice or C57BL 6 mice, the difference was statistically significant (P <0.01). Homomorphic mice prompted the most severe atherosclerotic lesions, followed by heterozygous offspring, and non-transgenic mice aortic atherosclerosis lesser. Transgenic mice liver and kidney can also be seen obvious lesions. This result suggests