[The role of syndecan-1 in the transformation of pulmonary epithelial stroma in rats with chronic obstructive pulmonary disease and its mechanism].

To explore the role and mechanism of polysaccharide-1 (syndecan-1) in the transformation of lung epithelial stroma (EMT) in rats with chronic obstructive pulmonary disease (COPD). Thirty male SD rats of clean grade were randomly divided into sham operation group (normal saline injection after tracheal exposure, =10), COPD group (fumigation after injection of 1 mg/ml lipopolysaccharide, transfection of 100 μl empty virus, =10) and syndecan-1 overexpression group (fumigation after injection of 1 mg/ml lipopolysaccharide, and transfection of 100 μl carrying rat syndecan-1 gene Ad-CMV-GFP-SDC1, =10), once a day for two weeks. After the treatment, the lung function was detected and lung tissues were collected. HE staining was used to observe lung injury. The expression levels of syndecan-1, vimentin and E-cadherin in lung tissue of rats in each group were detected by immunohistochemistry. Western blot was used to detect the expressions of TGF-β1, Smad2/3 and p-Smad2/3. The mRNA levels of vimentin, E-cadherin, TGF-β1 and Smad2/3 were detected by RT-PCR. Compared with the sham operation group, the airway mucosa of COPD group was exfoliated, the lumen was narrow, the airway wall was more inflammatory cell infiltration, emphysema was serious, expiratory volume (V), peak expiratory flow (PEF), Forced expiratory volume in 0.3 s (FEV) and the expression of E-cadherin mRNA were significantly decreased (＜0.05). While the expression of vimentin, TGF-β1 and Smad2/3 mRNA were increased, and the expression levels of TGF-β1, Smad2/3 and p-Smad2/3 protein were significantly increased (＜0.05). Compared with COPD group, the number of airway mucosa exfoliation and inflammatory cell infiltration in airway wall were decreased, lumen stenosis and emphysema were improved, the levels of V, PEF, FEV and the expression of E-cadherin mRNA were significantly increased (＜0.05). And the expressions of vimentin, TGF-β1 and Smad2/3 mRNA were decreased, and expression levels of TGF-β1, Smad2/3 and p-Smad2/3 protein were significantly decreased (＜0.05). In COPD rats, TGF-β/Smad signal pathway activation induced the production of EMT; overexpression of syndecan-1 could inhibit the EMT mediated by TGF-β/Smad signal pathway, and improve the lung tissue injury of COPD rats.