阿托伐他汀调节血管球囊损伤术后核受体Nur77的表达  

Atorvastatin regulated the expression of Nur77 in rat carotid artery postangioplasty restenosis model

作　　者：王丽岳 曾秋棠[1] 龚凡[1] 董晓燕[2] 毛奕[1] 

机构地区：[1]华中科技大学协和医院心内科,武汉430022 [2]武汉大学附属同仁医院心内科,武汉430060

出　　处：《临床心血管病杂志》2010年第7期540-544,共5页Journal of Clinical Cardiology

基　　金：武汉市卫生局科研基金项目[武卫2009(76)]

摘　　要：目的:建立鼠颈动脉再狭窄模型,观察阿托伐他汀对核孤儿受体Nur77表达水平的影响及其与血管平滑肌细胞增殖的关系。方法:100只SD雄性大鼠高脂饮食。喂养1周后随机分为3组:空白对照组(BC组),血管球囊损伤术组(CG组),血管球囊损伤术后药物组(AIG组)。应用免疫组织化学法,WesternBlot,RT-PCR分析血管组织中Nur77的表达。结果:大鼠颈动脉再狭窄模型中,Nur77高表达;阿托伐他汀降低Nur77表达,减少血管平滑肌细胞的增殖。结论:Nur77促进血管平滑肌细胞增殖。减少Nur77表达可能是治疗再狭窄的新的机制和治疗靶点。Objective：To investigate the effects of atorvastatin on the expression of Nur77 and relation with the proliferation of vascular smooth muscle cells （VSMCs）.Method：100 SD male rats with high fat diet,feeding after 1 week were randomly divided into three groups：control group （BC Group）,vascular balloon injury group （CG group）,vascular balloon injury with the drug group （AIG Group ）.By using rat carotid artery postangioplasty restenosis models,we investigated the effects of atorvastatin on the expression of Nur77 by immunohistochemistry,RT-PCR,and Western blot.Result：Nur77 was overexpressed in neointima,but down-regulated by atorvastatin in rat carotid artery postangioplasty restenosis models.Conclusion：Nur77 promotes VSMCs proliferation.Down-Regulation of Nur77 by atorvastatin suggests a novel therapy strategy for atherogenesis based on suppression of VSMCs proliferation.

关 键 词：动脉粥样硬化 阿托伐他汀 Nur77 血管平滑肌细胞增殖 再狭窄 

分 类 号：R543.1[医药卫生—心血管疾病]