科研之友
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摘要
Excessive airway remodelling that occurs as a consequence of repetitive injury-repair cycles plays an important role in the pathogenesis of chronic asthma. Our study aimed to determine whether anti-nerve growth factor (NGF) therapy plays a role in preventing airway remodelling via the transforming growth factor (TGF)-beta/Smad signaling pathway in a murine model of chronic asthma. TGF-beta(1) mRNA levels of were detected by quantitative real-time PCR (QRT-PCR). Histological examination and Masson's trichrome staining were used to evaluate pathological lung changes. The expression of TGF-beta(1), P-Smad(3), Smad(7), and the downstream mesenchymal markers Snail, Slug, and alpha-SMA were measured using immunohistochemistry staining and Western blotting. Functional blockade of NGF in the asthmatic mice dramatically prevented lung inflammation and airway remodelling. TGF-beta(1) and P-Smad(3) expression were decreased in the anti-NGF group. In bronchial epithelial cells, the TGF-beta/Smad-induced expression of the mesenchymal markers Snail, Slug, and alpha-SMA were inhibited by the anti-NGF antibody. NGF exerts profibrotic effects on airways, which might be mediated by the TGF-beta/Smad-induced epithelial-mesenchymal transition.
