瑞舒伐他汀对载脂蛋白E基因敲除小鼠血管内皮黏附性的影响  

Rosuvastatin attenuates vascular endothelial adhesiveness in apolipoprotein E-deficient mice

作　　者：李伟[1] 黄海英[2] 吴智勇[1] 谢方道[1] 张旭日[1] 管频[1] 

机构地区：[1]海南省人民医院老年病科干部医疗保健中心,海口570311 [2]海南省人民医院药学部,海口570311

出　　处：《中华心血管病杂志》2009年第1期69-72,共4页Chinese Journal of Cardiology

摘　　要：目的观察瑞舒伐他汀抗血管壁炎症的作用。方法载脂蛋白E基因敲除小鼠80只和C57BIM6小鼠20只，均为8～9周龄。分为2周药物处理组和6周药物处理组，每组各40只载脂蛋白E基因敲除小鼠和10只C57BL／6小鼠。载脂蛋白E基因敲除小鼠每日1次皮下注射不同浓度的瑞舒伐他汀，剂量分别为0、1、5和20mg／kg。药物处理满2周或6周时，心内穿刺取血，并收获小鼠主动脉。结果经瑞舒伐他汀处理2周或6周后，载脂蛋白E基因敲除小鼠血浆总胆固醇和低密度脂蛋白胆固醇明显下降，但甘油三酯和高密度脂蛋白胆固醇均无明显变化。经瑞舒伐他汀处理2周后，20mg／kg组载脂蛋白E基因敲除小鼠主动脉内皮一单核细胞黏附率有明显下降；经瑞舒伐他汀处理6周后，5、20mg／kg组载脂蛋白E基因敲除小鼠主动脉内皮一单核细胞黏附率均有明显下降。经定量RT—PCR分析，瑞舒伐他汀20mg／kg能明显抑制载脂蛋白E基因敲除小鼠主动脉VCAM-1、MCP．1mRNA表达。结论瑞舒伐他汀具有抑制动脉粥样硬化早期炎症反应的作用。Objective To investigate the anti-inflammatory effects on the vessel wall of rosuvastatin in apolipoprotein E-deficient mice. Methods Eight-week-old apolipoprotein E-deficient mice fed a normal chow diet were treated with vehicle or various doses of rosuvastatin （ 1, 5, or 20 mg/kg） by subcutaneous injection for 2 or 6 weeks prior to sacrifice. Endothelial adhesiveness for monoeytes was determined by functional binding assay. The expressions of vascular cell adhesion molecule-1 and monoeyte ehemotactic protein-1 in the vessel wall were detected by quantitative real-time polymerase chain reaction. Results Endothelial adhesiveness for monocytes was significantly attenuated after 2 or 6 weeks treatments with 5 or 20 mg/kg rosuvastatin. Rosuvastatin also significantly reduced the expressions of vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 in the vessel wall. Conclusion The anti-inflammatory effects of suvastatin might be responsible for attenuating the pathogenesis of atherogenesis in apolipoprotein E-deficient mice.

关 键 词：降血脂药 载脂蛋白E类 小鼠 基因敲除 

分 类 号：R686[医药卫生—骨科学]