香烟诱导的肺动脉重构过程中血管紧张素Ⅱ与转化生长因子-β1的相互影响和作用  

Effect of AngII and TGF-β1 on cigarette smoke-induced pulmonary arterioles remodeling

作　　者：韩素霞[1] 郭李平[1] 常建梅[1] 孙理华[1] 冯磊[1] 董晓光[1] 

机构地区：[1]新疆医科大学第五附属医院心血管内科,乌鲁木齐830011

出　　处：《新疆医科大学学报》2013年第12期1721-1723,共3页Journal of Xinjiang Medical University

基　　金：国家自然科学基金(81060023)

摘　　要：目的探讨香烟诱导的肺动脉高压形成过程中血管紧张素Ⅱ(AngiotensinⅡ,AngⅡ)与转化生长因子-β1(Transforming growth factor beta,TGF-β1)的相互影响和作用。方法建立香烟诱导的肺动脉高压大鼠模型,将48只健康雄性SD大鼠随机分为对照组、对照+氯沙坦组、香烟暴露组、香烟暴露+氯沙坦组。采用HE染色法观察肺动脉的病理变化;采用放射免疫法检测大鼠肺组织中AngⅡ蛋白水平;用Western blot法检测TGF-β1蛋白表达;给予氯沙坦干预后,检测AngⅡ通过TGF-β1对香烟诱导的大鼠肺动脉高压的作用。结果 6个月后,香烟暴露组大鼠肺小动脉出现重构改变;香烟暴露组大鼠肺组织匀浆中AngⅡ蛋白含量较对照组明显升高(P<0.05),香烟暴露组大鼠肺组织TGF-β1蛋白表达量显著升高(P<0.05),香烟暴露+氯沙坦组较香烟暴露组肺组织AngⅡ蛋白含量和TGF-β1蛋白表达均显著降低(P<0.05);肺小动脉重构得到改善。结论慢性香烟暴露导致肺小动脉重构,还可引起肺组织AngⅡ蛋白含量、TGF-β1蛋白表达水平升高而参与肺小动脉壁增厚及重构;氯沙坦可通过拮抗肺组织AngⅡ蛋白水平而抑制TGF-β1蛋白表达,进一步改善香烟诱导的肺动脉重构病变。Objective This study is to explore the potential role of Ang [[ and TGF-131 in cigarette-induced pulmonary arterioles remodeling. Methods Rats were randomly divided into four groups. The model groups were exposed to the smoke; after 6 months, lung morphology and tissue biochemical changes were examined by applying Western blotting and radioimmunoassay. Results The levels of lung tissue Ang Ⅱ increased in cigarette smoke-induced remodeling of small pulmonary arterioles in rats. The changes of Ang II were related to activation of TGF-β1, as shown by inhibition with losartan. Conclusion This study demonstrated that Ang Ⅱ and TGF-β1 played an essential role in cigarette-induced PAH.

关 键 词：香烟 肺动脉重构 血管紧张素Ⅱ 转化生长因子-Β1 

分 类 号：R363.14[医药卫生—病理学]