| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3447294 | Archives of Medical Research | 2008 | 9 Pages |
BackgroundSecretory leukocyte proteinase inhibitor (SLPI) is an important antileukoprotease in airway. The aim of the present study was to explore the expression of SLPI in the bronchi and lung tissues of chronic obstructive pulmonary disease (COPD) models and the regulative mechanism by transforming growth factor (TGF)β1/Smads signal pathway in bronchial epithelial cell.MethodsCOPD rat model was established and was treated with or without TGFβ1 monoclonal antibody. Spirometry was conducted, and expressions of TGFβ1, Smad4 and SLPI were examined by immunohistochemistry and reverse-transcription polymerase chain reaction (RT-PCR), respectively. The normal human bronchial epithelial cell (NHBE) was cultured, preincubated with or without siRNA (Smad4), and then stimulated with TGFβ1. Expressions of Smad4 and SLPI were detected by immunocytochemistry, Western blot and RT-PCR, respectively.ResultsAs compared with the model group, after treatment with TGFβ1 monoclonal antibody, peak expiratory flow (PEF), forced expiratory volume in 0.3 sec (FEV0.3) and FEV0.3/forced vital capacity (FVC) in the TGFβ1 monoclonal antibody intervention group were all significantly improved. Expression of SLPI was also improved, but expression of Smad4 was significantly decreased. Expression of SLPI in NHBE cells was inhibited by TGFβ1 both at the mRNA level and the protein level. Furthermore, effect of TGFβ1-inhibited expression of SLPI in NHBE cells was disengaged by siRNA (Smad4) both at the mRNA level and the protein level.ConclusionsDecreased expression of SLPI in the COPD rat model may be mainly caused by the increased expression of TGFβ1, and this process is probably related to the activation of Smads signal pathway.
