摘要
目的探讨TNFα及ICAM-1在COPD发病中的作用。方法采用熏香烟加气管内注射内毒素法复制大鼠COPD的动物模型,并测定了大鼠的肺功能及血气变化结果,用免疫组织化学法观察了TNFα及ICAM-1在肺组织中的表达情况。结果模型组动物均发生了不同程度的COPD,与正常对照组比较,模型组动物的MVV、PEF、FEV0.3、CL显著低于正常对照组,两者比较差异显著,P<0.05;模型组动物PaCO2高于对照组,PaO2及SaO2低于对照组,发生了明显的呼吸性酸中毒;TNFα及ICAM-1在正常对照组动物支气管上皮细胞中仅见微量的表达,在模型组的支气管上皮细胞、支气管周围的淋巴滤泡炎性细胞及肺泡间质炎性细胞可见到强阳性表达。结论TNFα及ICAM-1参与了COPD的发生及发展。
Objective:To explore the effect of TNF αand ICAM-1 in COPD Methods:using passive cigarette smoking plus intratracheal instillation of lipopolysacchide to reconstructed COPD model and detect the lung functions and bloody gas results,lung tissue Results:Model rats existed differently degree COPD,compared with controlled group,MVV、PEF、FEV0 3and CL were lower in experimental group There existed obvious difference between them,P < 0 05;compared with controlled group,PaCO2 was higher while PaCO2 and SaO2 were lower in experimental group,the rats occurred obviously acidosis;TNF αand ICAM-1 protein were tiny exprssed in the area of bronchial epithelium cells in controlled group TNF αand ICAM-1 protein were expressed strongly in the area of bronchial epithelium cells,lymph follicle inflammatory cells and alveolus inflammatory cells around bronchus in experimental group Conclusion:TNF αand ICAM-1 protein participated in COPD occurring and progressing
出处
《井冈山医专学报》
2004年第4期1-3,共3页
Journal of Jinggangshan Medical College
关键词
慢性阻塞性肺病
肿瘤坏死因子
细胞间黏附分子
chronic obstructive pulmonary disease
tumor necrosis factor
intercellular adhere molecul
