| Objectives:AS all we know, Chronic obstructive pulmonary disease will be the third cause in the world, which is endowed with by limitation of airflow-both into and out of the lungs-that is not fully recersible. Airflow limitation in COPD is progressive, meaning it generally worsens over" time. The inflammation in lung parenchyma and airway is considered to be the initiating factor of COPD, that will influence the pathological process of COPD. Airway remodeling leading to airflow limitation, increase of airway resistance or the airway obstruction, is an important pathologic feature of COPD.Cigarette smoke exposure combine with LPS induced models of COPD was taking in this study. COPD rats were administrated intragastricly by Feishuai mixture for two months. And then, lung morphology and levels of interleukin (IL-8), tumor necrosis factor (TNF-α),endothelin (ET-1) and superoxide dismutase (SOD) were determined to reflect the status of inflammation, while metal matrix protein 2 and 9 were determined by immunohistochemistry (IHC)Methods:36 rats were randomized into three groups include healthy control, COPD model and Feishuai. COPD rats, induced by cigarette smoke and LPS exposures for two months, was administrated intragastricly by saline or Feishuai mixture for another two months. And then, lung morphology and levels of interleukin (IL-8), tumor necrosis factor (TNF-a),endothelin (ET-1) and superoxide dismutase (SOD) were determined to reflect the status of inflammation, while metal matrix protein 2 and 9 were determined by immunohistochemistry (IHC)Result:Pathological changes:compared with COPD model group, the alveolar structure in the FeiShuai group was relatively complete, part of alveolar wall thinning, alveolar surface area reduction, decreased alveolar wall tissue density, alveolar pores to expand. Compared with the model group, the pulmonary emphysema formation of cystic cavity was smaller, the status of inflammation was lighter.ELISA results:Serum endothelium-1, TNF and IL-8 in bronchoalveolar lavage fluid were determined:Compared with the control group, three kind of inflammatory cytokine in COPD model group was significantly increased, the difference was statistically significant (P<0.05);While compared with the model group, the inflammatory cytokine was significantly decreased in FeiShuai mixture group, (P<0.05). There were no significant difference in SOD between the groups.Immnohistochemistry results:Compared with the healthy control group, model control groups of matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) was significantly increased, (P< 0.05); Compared to the model group, the FeisShuai groups of rats pulmonary tissue matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) significantly decreased, (P<0.05).Thickness of airway smooth muscle:Compared with the healthy control group, the smooth muscle layer was thicker in the model control groups (P<0.05); Compared to the model group, the smooth muscle layer was thinner in the FeisShuai groups of (P<0.05).Conclusion:There are more inflammatory cells in lung tissue, the degree of lung injury is more severe than other groups.Application of FeiShuai mixture can reduce inflammatory cytokines levels include bronchial bronchoalveolar lavage IL-8, TNF alpha and plasma ET-1,thereby reducing the inflammation of the lung tissue.But on the SOD activity in lung homogenate FeiShuai mixture shows no obvious effect. FeiShuai mixture shows obvious effect on the level of in MMP-2, MMP-9 expression, reducing small airway wall thickness of bronchial smooth muscle. FeiShuai mixture shows potential in reducing the protease and improving airflow limitation and airway remodeling, slowing the progression of chronic obstructive pulmonary disease (COPD). |