中国组织工程研究与临床康复2011，Vol.15Issue(41)：7647-7652,6.DOI:10.3969/j.issn.1673-8225.2011.41.012
门静脉高压征模型大鼠构建及门静脉侧支血管和内脏血管的形成
Portosystemic collateral vessel and splanchnic vessel formation in a rat model of portal hypertension
摘要
Abstract
BACKGROUND: The Apelin/APJ system has been confirmed to decrease blood pressure, strengthen systole and Apelin can stimulate angiogenesis. OBJECTIVE: To determine the expression of apelin and APJ in splanchnic tissues, and to test if apelin has a pathophysiological role in the development of splanchnic neovascularization, splanchnic hyperemia, and portosystemic collateralization in a rat model of portal hypertension. METHODS: Partial portal vein-ligated rats were treated with the APJ antagonist F13A for 7 days. Splanchnic neovascularization and expression of angiogenesis mediators (western blotting) were determined. Portosystemic collateral formation (microspheres) and hemodynamic parameters (ow cytometry) were also assessed. RESULTS AND CONCLUSION: Apelin and its receptor APJ were overexpressed in the splanchnic vasculature of portal hypertensive rats. F13A effectively decreased, by 52%, splanchnic neovascularization and expression of proangiogenic factors vascular endothelial growth factor, platelet derived growth factor, and angiopoietin-2 in portal hypertensive rats. F13A also reduced, by 35%, the formation of portosystemic collateral vessels. These findings suggest that the apelin/APJ system contributes to portosystemic collateralization and splanchnic neovascularization in portal hypertensive rats, presenting a potential novel therapeutic target for portal hypertension.关键词
血管生成/血管内皮生长因子/门静脉压力/apelin/APJ/大鼠分类
医药卫生引用本文复制引用
毛小环,戴文建,杨莉,柳威..门静脉高压征模型大鼠构建及门静脉侧支血管和内脏血管的形成[J].中国组织工程研究与临床康复,2011,15(41):7647-7652,6.基金项目
国家自然科学基金项目(30901577),教育部留学回国人员科研启动基金(20091590),湖南省教育厅项目(11C0469). （30901577）
