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生长反应因子与大鼠颈动脉损伤后内膜增生*★

王帅 刘闺男 王泰然

中国组织工程研究Issue(7):1233-1237,5.
中国组织工程研究Issue(7):1233-1237,5.DOI:10.3969/j.issn.2095-4344.2013.07.017

生长反应因子与大鼠颈动脉损伤后内膜增生*★

Decoy oligodeoxynucleotides and neointimal hyperplasia following balloon injury of rat common carotid artery

王帅 1刘闺男 1王泰然1

作者信息

  • 1. 中国医科大学附属第一医院心内科,辽宁省沈阳市110001
  • 折叠

摘要

Abstract

BACKGROUND: Restenosis fol owing percutaneous coronary intervention is stil a clinical y serious problem which negatively affects the long-term therapeutic benefit of percutaneous coronary intervention. OBJECTIVE: To investigate the effect of Egr-1 decoy oligodeoxynucleotides via intracerebroventricular injection on the neointima after carotid bal oon injury and to primarily study its mechanism of inhibiting neiointimal hyperplasia, thus providing a new prospect to find a new target of vascular remodeling and restenosis. METHODS: Endothelial denuded carotid models were prepared in rats by bal oon withdrawal injury with the help of 2F Fogarty. Then Egr-1 decoy oligodeoxynucleotides were injected into injured vascular subsection which was mediated by Fugene6 transfection reagent. The extent of neointimal hyperplasia and the expression of Cyclin D1 were detected by hematoxylin-eosin staining and immunohistochemistry, respectively.RESULTS AND CONCLUSION: Neointimal hyperplasia was significantly inhibited by Egr-1 decoy oligodeoxynucleotides. The expression of Cyclin D1, which was dramatical y increased after bal oon injury of rat common carotid artery, was significantly down-regulated by Egr-1 decoy oligodeoxynucleotides. Egr-1 decoy oligodeoxynucleotides may inhibit neointimal hyperplasia fol owing bal oon injury of rat common carotid artery via down-regulation of Cyclin D1.

关键词

组织构建/组织构建与生物活性因子/生长反应因子/颈动脉/损伤/诱骗寡脱氧核苷酸/Cyclin D1/球囊损伤/再狭窄/国家自然科学基金/组织构建图片文章

分类

医药卫生

引用本文复制引用

王帅,刘闺男,王泰然..生长反应因子与大鼠颈动脉损伤后内膜增生*★[J].中国组织工程研究,2013,(7):1233-1237,5.

基金项目

国家自然科学基金项目(30871074)。Supported by:the National Natural Science Foundation of China, No.30871074* (30871074)

中国组织工程研究

OACSCDCSTPCD

2095-4344

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