非活性型脂蛋白脂酶在动脉粥样硬化早期病变形成中的作用  

Role of inactive lipoprotein lipase in the development of early atherosclerosis after arterial balloon injury in rabbit

作　　者：吴晓君[1] 胡蓉[2] 刘朝中[1] 黄从春[1] 

机构地区：[1]空军总医院心血管内科,北京100036 [2]空军总医院肿瘤科,北京100036

出　　处：《中国心血管杂志》2011年第1期34-37,共4页Chinese Journal of Cardiovascular Medicine

摘　　要：目的探讨兔动脉壁高表达非活性型脂蛋白脂酶(LPL)在动脉粥样硬化发生中的作用。方法新西兰兔24只,以腺病毒基因转移技术转染基因,随机分为3组,以碱性磷酸酶(AP)基因作对照(对照组),通过球囊导管损伤兔颈总动脉造模后,实验组在血管壁高表达活性型人LPL(hLPL组),非活性型人LPL_(194)基因(hLPL_(194)组)。1周后通过油红O染色及免疫组化对血管壁的形态进行分析。结果 hLPL_(194)组血管壁内膜下有明显的脂质沉积,定量分析显示较对照组增高(0.0545±0.0097比0.012±0.0004)(P<0.01),但较hLPL组少(0.1043±0.0462)(P<0.01)。同时发现hLPL_(194)组的动脉壁内膜下局部巨噬细胞浸润与hLPL组一样也有增多。而3组动物的血浆总胆固醇、三酰廿油及高密度脂蛋白胆固醇水平差异均无统计学意义(均为P>0.05)。结论非活性型LPL和活性型LPL一样,在血管壁内膜下过表达时,能引起内膜下脂质沉积,并伴有巨噬细胞浸润,促进动脉粥样硬化早期病变的形成。Objective To assess the role of inactive lipoprotein lipase （LPL） over expression in atherogenesis in rabbit. Methods Twenty-four New Zealand white rabbits were randomly divided into 3 groups. The carotid arteries of rabbits were infected with adenovirus （Ad） containing either human wild type I,PL, or inactive LPL194 or alkaline phosphatase （AP） after balloon injury. Lipid deposit, and infiltration of macrophage were analyzed by Oil Red O （ORO） staining and immunochemistry method. Results Compared with AP group （0. 012±0. 0004 ） , lipids in sub-endothelial space in injured carotid artery （ORO positive） increased significantly in rabbits infected with Ad-LPL （0. 1043±0. 0462） or Ad-LPL194 （ 0. 0545±0. 0097 ） and macrophage infiltration increased significantly as well. There were no significant changes of plasma cholesterol, triglycerides and HDL-C among the three groups. Conclusion Over expression of inactive human LPL194 in balloon injured carotid artery of rabbits can promote early atherosclerotic lesion formation.

关 键 词：酯酶类 动脉粥样硬化 黏脂质累积病 

分 类 号：R543.5[医药卫生—心血管疾病]