血管外膜损伤后血管组织氧化应激与内膜病变

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.

Oxidative stress and intimal hyperplasia lesion in vascular tissues after vascular adventitial injury

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.