摘要
目的探讨TNFα及TNFαmRNA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,用免疫组织化学及原位杂交法观察了TNFα及Mrna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Mrna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Mrna参与了COPD的发生及发展.
ObjectiveTo explore the effect of TNFα and TNFα mRNA in COPD.MethodsUsing passive cigarette smoking and intratracheal instillation of lipopolysacchide reconstructed COPD model and detected the lung functions and changing results of bloody gas, TNFα and its mRNA expression in lung tissue are observed by using immunohistochemical and hybridization in situ methods.ResultsModel rats existed different degrees of COPD, compared with control group, MVV, PEF, FEV(0.3) and CL were lower than those of experimental group. There existed obvious difference between of them, P<(0.05);compared with controlled group, PaCO_2 was higher while PaO_2 and SaO_2 were lower in experimental group, the rats occurred obviously respiratory acidosis; TNFα and its mRNA protein were tiny expressed in the area of bronchial epithelium cells in controlled group. TNFα and its mRNA protein were expressed strongly in the area of bronchial epithelium cells, lymph follicle inflammatory cells and alveolus inflammatory cells around bronchus in experimental group.ConclusionTNFα protein and its mRNA participated in COPD occurring and progressing.
出处
《北华大学学报（自然科学版）》
CAS
2004年第5期408-411,共4页
Journal of Beihua University（Natural Science）
基金
吉林省科技厅科研基金项目(2004031 09)
