Background Chronic obstructive pulmonary disease （COPD） is associated not only with airway inflammation characterized by mucin hypersecretion but also with systemic inflammation. Tumor necrosis factor alpha （TNF-α...Background Chronic obstructive pulmonary disease （COPD） is associated not only with airway inflammation characterized by mucin hypersecretion but also with systemic inflammation. Tumor necrosis factor alpha （TNF-α） is found to take part in systemic inflammation, and ErbB3 plays an important role in mucin hypersecretion of COPD. Since TNF-α converting enzyme （TACE） is involved in the activation of both TNF-α and ErbB3, we established rat models of COPD to investigate the expressions of TACE, TNF-α and ErbB3 and to explore the correlations among TACE,TNF-α and ErbB3 respectively. Methods Thirty Wistar male rats were randomly divided into COPD group （group C, n=10）, saline solution parallel group （group P, n=-8）, and normal control group （group N, n=-8）. Group C was challenged with passive cigarette smoking and intratracheal instillation of lipopolysaccharide. Six weeks later pulmonary functions were tested, bronchoalveolar fluid and arterial blood gases were assayed, and histopathological evaluations were performed in turn. The expressions of TACE, TNF-α and ErbB3 in lungs of all rats were determined histochemically. Results The expressions of TACE, TNF-α and ErbB3 were significantly higher in group C than in group N （P〈0.01）. The contents of TNF-α in serum （P〈0.01） and bronchoalveolar lavage fluid （BALF） （P〈0.01） were elevated more significantly in group C than in group N. A positive correlation existed between TACE and TNF-α （r=0.784, P〈0.01） and between TACE and ErbB3 （r=0.526, P〈0.01） respectively. Conclusions TNF-α and ErbB3 are involved in the pathogenesis of COPD. TACE contributes to the progress of COPD indirectly through the function of TNF-α and ErbB3.展开更多
文摘Background Chronic obstructive pulmonary disease （COPD） is associated not only with airway inflammation characterized by mucin hypersecretion but also with systemic inflammation. Tumor necrosis factor alpha （TNF-α） is found to take part in systemic inflammation, and ErbB3 plays an important role in mucin hypersecretion of COPD. Since TNF-α converting enzyme （TACE） is involved in the activation of both TNF-α and ErbB3, we established rat models of COPD to investigate the expressions of TACE, TNF-α and ErbB3 and to explore the correlations among TACE,TNF-α and ErbB3 respectively. Methods Thirty Wistar male rats were randomly divided into COPD group （group C, n=10）, saline solution parallel group （group P, n=-8）, and normal control group （group N, n=-8）. Group C was challenged with passive cigarette smoking and intratracheal instillation of lipopolysaccharide. Six weeks later pulmonary functions were tested, bronchoalveolar fluid and arterial blood gases were assayed, and histopathological evaluations were performed in turn. The expressions of TACE, TNF-α and ErbB3 in lungs of all rats were determined histochemically. Results The expressions of TACE, TNF-α and ErbB3 were significantly higher in group C than in group N （P〈0.01）. The contents of TNF-α in serum （P〈0.01） and bronchoalveolar lavage fluid （BALF） （P〈0.01） were elevated more significantly in group C than in group N. A positive correlation existed between TACE and TNF-α （r=0.784, P〈0.01） and between TACE and ErbB3 （r=0.526, P〈0.01） respectively. Conclusions TNF-α and ErbB3 are involved in the pathogenesis of COPD. TACE contributes to the progress of COPD indirectly through the function of TNF-α and ErbB3.
