【打印本页】 【下载PDF全文】 【HTML】 查看/发表评论下载PDF阅读器关闭

←前一篇|后一篇→

过刊浏览    高级检索

本文已被:浏览 3526次   下载 2215 本文二维码信息
码上扫一扫!
血管外膜损伤后血管组织氧化应激与内膜病变
汤月霞1,梁春2,刘永2,吴宗贵2*
0
(1.济南军区青岛第一疗养院,青岛 266071;2.第二军医大学长征医院心血管内科,上海 200003)
摘要:
目的:探讨NADPH氧化酶相关的氧化应激在外膜损伤致内膜病变中的作用。方法:选用纯种新西兰大白兔,采用胶原酶消化+钝性机械分离的方法建立血管外膜损伤动物模型,采用H-E染色观察外膜损伤血管的形态变化,实时荧光定量PCR(real-time quantitative PCR,RQ-PCR)技术检测外膜损伤后血管组织NADPH氧化酶亚单位p22phox、抗氧化酶HO-1的mRNA表达,荧光探针检测外膜损伤后血管组织活性氧(reactive oxygen species,ROS)的生成。结果:外膜损伤可致内膜增生性病变;外膜损伤导致p22phox/HO-1 mRNA表达明显升高,血管组织ROS产量增加。结论:血管外膜参与了内膜病变形成的病理过程;NADPH氧化酶活性升高导致的氧化应激可能是外膜损伤致内膜病变的机制之一。
关键词:  血管外膜损伤  氧化应激  NADPH氧化酶  活性氧  动脉粥样硬化
DOI:10.3724/SP.J.1008.2008.00912
投稿时间:2007-11-22修订日期:2008-04-02
基金项目:国家重点基础研究规划(“973”计划)(2005CB523309).
Oxidative stress and intimal hyperplasia lesion in vascular tissues after vascular adventitial injury
TANG Yue-xia1,LIANG Chun2,LIU Yong2,WU Zong-gui2*
(1.The First Sanitorium of Qingdao,PLA Jinan Military Area Command,Qingdao 266071,China;2.Department of Cardiology,Changzheng Hospital,,Second Military Medical University,Shanghai 200003)
Abstract:
Objective:To assess the role of NADPH oxidase-related oxidative stress in the intimal hyperplasia induced by adventitial injury.Methods: Animal model of vascular adventitial injury was established by combining collogenase digestion and mechanical dissection.HE staining was used to observe the morphological changes of the vessels after adventitial injury; RT-PCR was used to examine the mRNA expression of NADPH oxidase subunit p22phox and antioxidant heme oxygenase-1; and fluorescence probe was employed to detect the ROS production in the vessels.Results: Adventitial injuries could induce intimal hyperplasia lesions in the vessels;they also led to the elevated expression of p22phox/HO-1 mRNA and increased production of ROS.Conclusion: The vascular adventitia is involved in the pathological process of intimal hyperplasia,and oxidative stress caused by increased NADPH oxidase activity may be one of the mechanisms.
Key words:  adventitia  oxidative stress  NADPH oxidase  reactive oxygen species  atherosclerosis