中国动脉硬化杂志2013，Vol.21Issue(1)：6-10,5.
CBP基因沉默对大鼠颈动脉球囊损伤后内膜增生的影响
Effect of CREB Binding Protein Silencing on Neointimal Hyperplasia in Rat Carotid Arteries After Balloon Injury
摘要
Abstract
Aim To investigate the effects of siRNA recombinant lentivirus targeting CREB binding protein (CBP) gene on neointimal hyperplasia in rat carotid arteries after balloon injury and its possible mechanism. Methods Forty-eight male SD rats were randomly divided into four groups; Sham group, PBS group, CBP-siRNA-Lentivirus group and NC-siRNA-Lentivirus group to establish the model of balloon-injury in left common carotid artery, and the rats were sacrificed 28 days after injury and in vivo gene transfer. The expression of CBP and acetylated nuclear factor kappaB p65 ( NF-KB p65 ) were determined by real-time PCR and Western Blot. Proliferating cell nuclear antigen ( PCNA ) protein expression was detected by immunohistochemistry. Meanwhile, morphometric analysis was used to measure neointimal hyperplasia. Results 28 days after operations, lentivirus siRNA targeting CBP markedly decreased CBP mRNA and protein expression compared with PBS and NC-siRNA-Lentivirus groups ( P ＜ 0. 05 ). CBP gene silencing significantly reduced the neointimal area (0. 108 ±0. 008 mm2 vs 0. 238 ±0. 022 mm2 and 0. 252 ±0. 016 mm2, P ＜0. 05) and intima / media ratio (0. 706 ±0. 062 vs 1. 483 ±0. 136 and 1. 497 ±0. 137, P ＜0. 05). Furthermore, compared with PBS and NC-siRNA-Lentivirus groups, PCNA and acetylation of NF-kB p65 expression were both obviously downregulated in CBP-siR-NA-Lentivirus group ( P ＜ 0. 05 ) . Conclusions Lentivirus-mediated CBP gene silencing could efficiently suppress neointimal formation in balloon injured rat carotid artery, and the mechanism was involved with downregulation of NF-κB p65 acetylation.关键词
CREB结合蛋白/基因沉默/内膜增生/核因子κB/乙酰化Key words
CREB Binding Protein/ Gene Silencing/ Neointimal Hyperplasia/ Nuclear Factor KappaB p65 / Acetylation分类
医药卫生引用本文复制引用
杨简,江洪,杨俊,丁家望,李松,陈静..CBP基因沉默对大鼠颈动脉球囊损伤后内膜增生的影响[J].中国动脉硬化杂志,2013,21(1):6-10,5.基金项目
国家自然科学基金资助项目(81200088和30770849) （81200088和30770849）
湖北省自然科学基金资助项目(2011CDB179) （2011CDB179）
