摘要
目的通过测定COPD大鼠血清及肺组织中CC16的水平,探讨烟熏在COPD形成中的作用。方法采用烟熏加气管内注入内毒素法建立大鼠COPD模型。HE染色观察大鼠肺、支气管的病理改变。ELISA法检测血清中CC16的含量。免疫组化法检测肺组织中CC16的含量变化。结果 COPD组大鼠血清及肺组织中CC16含量与对照组相比均明显降低(P<0.01);内毒素组大鼠血清及肺组织中CC16含量较对照组低,但差别无统计学差异。结论香烟烟熏造成COPD大鼠血清及肺组织中CC16的含量降低,这一改变可能是吸烟所致COPD形成的机制之一。
Objective To explore the impacts of tobacco smoking on the pathogenesis of chronic obstructive pulmonary disease （COPD） by testing the changed levels of CC16 in serum and pulmonary tissues of COPD mice. Methods COPD mice model was estab- lished with the airway infused with lipopolysaccharide （LPS） and inhaled by cigarette smoke （CS）. We used Hemotoxylin-eosin （HE） staining to investigate the pathological changes in the lung and bronchus, ELISA to measure CC16 levels in serum, and immunohistochem- istry to test CC16 levels in the pulmonary tissues. Results Compared with the control group, a remarkable decrease of CC16 levels in the serum and lung tissues was identified in the COPD groups （P 〈0. 01 ）. The CC16 levels were lower in the LPS mice than those in the con- trol group, but no statistical differences. Conclusion The change of CC16 levels in serum and pulmonary tissues of COPD mice suggests that CS might be one of the mechanisms underlying the development of COPD.
出处
《临床肺科杂志》
2012年第8期1370-1372,共3页
Journal of Clinical Pulmonary Medicine
基金
2010年南京市卫生局科技发展计划(TKK10103)
