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目的研究环境因素中臭氧与慢性阻塞性肺病发病率升高之间的关系;探讨臭氧暴露对COPD个体气道炎症及肺组织NF-κB P65蛋白表达的影响。方法雄性SD大鼠30只,随机分为三组,对照组,COPD模型组,模型叠加臭氧暴露组,每组10只。每日熏吸香烟和两次气管内滴入200ug脂多糖建立大鼠COPD模型,模型加臭氧暴露组在此基础上进行1次急性臭氧暴露,暴露时间为4h。观察记录各组大鼠一般情况,HE染色检测大鼠肺组织病理改变,支气管肺泡灌洗液行瑞士染色,显微镜下进行炎症细胞分类计数,免疫组化检测肺组织NF-κB P65蛋白表达量。结果模型组大鼠的肺组织损伤及病理变化总分显著高于对照组大鼠(P<0.01),臭氧组总分显著高于模型组(P<0.01);模型组大鼠BALF(支气管肺泡灌洗液)中炎性细胞总数高于对照组,臭氧组高于模型组;模型组大鼠肺组织NF-κB P65蛋白表达量显著高于对照组(P<0.01),臭氧组则显著高于模型组(P<0.05)。结论臭氧暴露可显著加重COPD气道炎症及NF-κB在肺组织中的表达。
Objective To study the relationship between ozone and chronic obstructive pulmonary disease (OS) in environmental factors. To investigate the effect of ozone exposure on airway inflammation and expression of NF-κB P65 in COPD patients. Methods Thirty male Sprague Dawley rats were randomly divided into three groups: control group, COPD model group and model group with ozone exposure group, with 10 rats in each group. The rats were smoked cigarettes twice a day, and twice intraperitoneal instillation of 200ug lipopolysaccharide in rats COPD model, the model plus ozone exposure group on this basis, an acute exposure to ozone, exposure time of 4h. The general conditions of rats in each group were observed and recorded. The pathological changes in lung tissue of rats were observed by HE staining. The bronchoalveolar lavage fluid was stained with Swiss. The number of inflammatory cells was counted under microscope. The expression of NF-κB P65 protein in lung tissue was detected by immunohistochemistry. Results The total score of lung injury and pathological changes in model group was significantly higher than that in control group (P <0.01), and the total score of ozone group was significantly higher than that of model group (P <0.01) Lavage fluid), the total number of inflammatory cells in the ozone group was higher than that in the control group. The expression of NF-κB P65 protein in the lung tissue of the model group was significantly higher than that of the control group (P <0.01) In model group (P <0.05). Conclusion Ozone exposure can significantly increase the airway inflammation and the expression of NF-κB in the lungs of COPD patients.