【摘要】 目的:通过观察一氧化氮合酶(NOS)在大鼠慢性阻塞性肺疾病(COPD)模型肺内的表达与分布,探讨其在吸烟导致COPD中的作用机制。方法:30只健康雄性二级SD大鼠随机分为健康对照组(15只)和COPD模型组(15只),采用烟熏加气管内滴入猪胰蛋白酶(PPE)联合的方法建立大鼠COPD模型,COPD模型制备后,行肺组织病理学检查;应用免疫组化方法观察肺内内皮型NOS(eNOS)、诱导型NOS(iNOS)的表达情况,且应用显微-微机图像处理系统进行定量分析。结果:联合应用烟熏和PPE在较短的时间内建立了较理想的COPD模型;一氧化氮合酶在正常肺组织与COPD的肺组织均有表达,主要定位在细胞浆内;免疫组化结果表明模型组iNOS在支气管黏膜上皮呈强阳性表达,肺血管eNOS表达明显减弱,与健康对照组比较有显著性(P<0.01)。结论:吸烟可引起iNOS的过量表达,引起肺部损伤,导致COPD的发生;同时大量吸烟可导致肺血管eNOS的表达减弱。更多还原

【Abstract】 Objective: To observe the expression of nitric oxide synthases in rat models with chronic obstructive pulmonary disease to study the mechanism of COPD caused by smoking.Motheds: 30 male Wistar rats were randomly divided into two groups,the normal control group(A,n=15)and the model group (B,n=15).COPD model(model group) was established by endotracheal instillation of pancreas protein enzyme with exposure to cigarette smoke in very short time.After COPD model had been established,pulmonary and bronchial morphological changes were observed by light and electron microscopy.The quantitative pathological examination by image analysis was also performed.The expression of inducible NOS(iNOS) and endothelial NOS(eNOS) in inpulmonary tissue was observed by immunohistochemistry techniques.Results: We estalished ideal COPD models in stort time.There existed the expression of NOS in both the normal lung tissue and the lung tissue of COPD,mainly orienrared in the cytoplasm of cell.The immunohistochemical result indicated that iNOS increased significantly,in comparison with the control group,in bronchiolar mycoderma epithelial and eNOS remakably decreased in pulmonary blood vessel.The expression of iNOS and eNOS were also markedly elevared(P<0.01).Conclusion: Smoking can induce overexpression of iNOS in pulmonary tissue,which might result in lung injury,COPD and weak expression of Enos in the pulmonary vessel.更多还原