Objective: To study the expression of secretory leukocyte proteinase inhibitor (SLPI) in the bronchi and lung tissues of chronic obstructive pulmonary disease (COPD) rat models and the regulatory mechanism by transforming growth factor beta(1) (TGF-beta(1)).
Methods: Rat COPD models were established by intratracheal instillation of lipopolysaccharide (LPS) twice and exposure to cigarette smoke daily. The drug intervention group received TGF-beta(1) monoclonal antibody 0.5 mg twice via tail venous injection. Spirometry was conducted and the pathological changes were observed. The concentrations of SLPI in bronchoalveolar lavage fluid (BALF) was measured by enzyme-linked immunosorbent assay (ELISA), the expressions of TGF-beta(1), Smad4 and SLPI in the bronchi and lung tissues examined by immunohistochemistry, and the expressions of TGF-beta(1) mRNA, Smad4 mRNA and SLPI mRNA in the bronchi and lung tissues detected by reverse transcription-polymerase chain reaction (RT-PCR).
Results: The SLPI positive coefficient, SLPI mRNA IOD value and the concentration of SLPI in BALF were significantly lower in the model group [(1.07), (0.17 +/- 0.01), (47 +/- 4) microg/L, respectively] as compared to the control group [(3.86), (0.84 +/- 0.10), (82 +/- 7) microg/L, respectively]. The TGF-beta(1) positive coefficient and the TGF-beta(1) mRNA IOD value were higher in the model group [(3.91), (0.71 +/- 0.09) respectively]than the control group [(1.12), (0.15 +/- 0.01), respectively]. After treated with TGF-beta(1) monoclonal antibody, the SLPI positive coefficient, SLPI mRNA IOD value and the concentration of SLPI in BALF were all significantly increased [(2.69), (0.59 +/- 0.05), (69 +/- 6) microg/L, respectively]. The PEF, FEV(0.3) and FEV(0.3)/FVC were all significantly improved in the drug intervention group [(28 +/- 6) ml/s, (4.4 +/- 1.3) ml, (80 +/- 10)%, respectively] as compared to the model group [(23 +/- 5) ml/s, (3.3 +/- 1.4) ml, (62 +/- 9)%, respectively].
Conclusion: The expression of SLPI in the COPD rat models significantly decreased, which may be caused by the increased expression of TGF-beta(1), and this process is probably related to the activation of Smads signal pathway.
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