摘要
Objective： To observe effects of Fengbaisan （丰白散, FBS） on the expression of matrix metalloproteinase-9 （MMP-9） and tissue inhibitor of metalloproteinase-1 （TIMP-1） in lung tissue of rats with chronic obstructive pulmonary disease （COPD） and to investigate the preventive and therapeutic mechanisms of FBS. Methods： The COPD rat model was established by cigarette smoke exposure and lipopolysaccharide （LPS） intra-tracheal dripping. The histopathological changes of lung tissue was observed via hematoxylin/eosin staining. The expression of MMP-9 and TIMP-1 in lung tissue was measured by reverse transcription polymerase chain reaction （RT-PCR） and immunohistochemistry. Results： The typical histopathological changes of COPD were displayed in the model group, Ambroxol Hydrochloride group and FBS group, and the pathological lesions in the FBS group were less than those in the model group. The expression of MMP-9 and TIMP-1 in the model group increased significantly compared with those in the normal group （P〈0.05）. After treatment for successive 28 days, the expression of MMP-9 and TIMP-1 in the FBS group decreased remarkably as compared with the model group （P〈0.05）. Conclusions： FBS can regulate MMP-9/TIMP-1 imbalance to prevent airway and lung parenchyma remodeling process via reducing the expression of MMP-9 and TIMP-1 in the lung tissue of COPD rats, and this may be a possible therapeutic mechanism of FBS on COPD. KEYWORDS chronic obstructive pulmonary disease, Fengbaisan, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, airway remodeling, Chinese medicine
Objective： To observe effects of Fengbaisan （丰白散, FBS） on the expression of matrix metalloproteinase-9 （MMP-9） and tissue inhibitor of metalloproteinase-1 （TIMP-1） in lung tissue of rats with chronic obstructive pulmonary disease （COPD） and to investigate the preventive and therapeutic mechanisms of FBS. Methods： The COPD rat model was established by cigarette smoke exposure and lipopolysaccharide （LPS） intra-tracheal dripping. The histopathological changes of lung tissue was observed via hematoxylin/eosin staining. The expression of MMP-9 and TIMP-1 in lung tissue was measured by reverse transcription polymerase chain reaction （RT-PCR） and immunohistochemistry. Results： The typical histopathological changes of COPD were displayed in the model group, Ambroxol Hydrochloride group and FBS group, and the pathological lesions in the FBS group were less than those in the model group. The expression of MMP-9 and TIMP-1 in the model group increased significantly compared with those in the normal group （P〈0.05）. After treatment for successive 28 days, the expression of MMP-9 and TIMP-1 in the FBS group decreased remarkably as compared with the model group （P〈0.05）. Conclusions： FBS can regulate MMP-9/TIMP-1 imbalance to prevent airway and lung parenchyma remodeling process via reducing the expression of MMP-9 and TIMP-1 in the lung tissue of COPD rats, and this may be a possible therapeutic mechanism of FBS on COPD. KEYWORDS chronic obstructive pulmonary disease, Fengbaisan, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, airway remodeling, Chinese medicine
基金
Supported by the Scientific Research Foundation of Traditional Chinese Medicine of Hunan Provincial Health Bureau(No.201194)
the General Science and Technology Project of Hunan Provincial Science and Technology Bureau(No.2011 SK3232)
