中文摘要：

目的观察血清淀粉样P蛋白（serllmamyloidPcomponent，SAP）缺失对小鼠动脉粥样硬化形成的影响。方法构建载脂蛋白E（ApolipoproteinE）和SAP双基因敲除小鼠（ApoE-/-；SAP-/-）作为实验组，ApoE“一小鼠作为对照组。2组小鼠各12只，组内雄雌小鼠各半。在小鼠第8周龄时，体质量约20g，此时开始同时给予2组小鼠高脂饮食，于第16周龄时获取小鼠全血分离得到血清进行血脂分析，处死小鼠后获取其心脏，胸腹主动脉进行油红O染色并进行病理统计。结果双基因敲除小鼠组的高密度脂蛋白胆固醇（HDL—C）明显高于对照小鼠（P〈0．01），低密度脂蛋白和高密度脂蛋白的比值和动脉粥样硬化指数（AI）小于对照组小鼠且差异显著（P〈0．01），而总胆固醇（TC），甘油三酯（TG）和低密度脂蛋白胆固醇（LDL．C）浓度无显著性差异（P〉0．05）；主动脉根部切片和胸腹主动脉的油红0染色结果表明SAP缺失明显减轻了小鼠动脉粥样硬化斑块面积（P〈0．01）。结论AP缺失可能通过上调HDL从而抑制ApoE。一小鼠动脉粥样硬化斑块形成。

英文摘要：

Objective To observe the effect of serum amyloid P component （SAP） deficiency on ath erosclerosis （AS）in mice. Methods Apolipoprotein E （ApoE） and SAP knockout mice served as an experimental group （n = 12） and ApoE knockout mice served as a control group （n = 12）. Their average body weight was about 20 g at the age of 8 weeks. The animals were then fed with high fat diet and killed at the age of 16 weeks. Blood, heart, and thoracico-abdominal aorta tissue samples were taken. Serum lipid was analyzed and the AS lesion Plaque area was measured after oil red O staining. Results The HDL-C level was significantly higher while the LDL-C/HDL-C value and atherogenic index（ AI）were significantly lower in experimental group than in control group（ P 〈 0. 01 ）. However, no significant difference was observed in TC, TG and LDL-C levels between the two groups （ P 〉 0. 05 ）. Oil red O staining showed that SAP deficiency significantly reduced the area of atherosclerosis plaques in heart and thoracico-abdominal aorta tissue samples （ P 〈 0. 01 ）. Conclusion SAP deficiency inhibits formation of atherosclerosis plaques in mice by up-regulating their HDL-C level.