Aerosol inhalation of ameliorates airway structural remodeling in chronic asthma mouse model.

Airway remodeling is accepted to be a determining component within the natural history of asthma. Nebulized inhalation of () has a protective effect on asthmatic mice. However, little is known regarding the effect of on airway structural remodeling in asthmatic mice. The purpose of this study was to explore the effect and the underlying mechanism of aerosol inhalation on airway structural remodeling in an asthma mouse model. Chronic asthma mouse models were established by ovalbumin induction. The number of inflammatory cells in bronchoalveolar lavage fluid (BALF), pathological alterations in lung tissue, and levels of associated cytokines (IL-5, IL-13, TNF-α, and ovalbumin-specific immunoglobulin E [OVA-sIgE]) were all assessed after therapy. The relative expression of interleukin (IL)-1β, tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), and Wnt1-induced signaling protein 1 (WISP1) mRNA were detected. Western blotting and immunohistochemistry detected the expression of Wnt/β-catenin pathway-related proteins in lung tissue. aerosol inhalation relieved airway inflammation, airway hyper-responsiveness, and airway remodeling. reduced the levels of IL-5, IL-13, TNF-α, and OVA-sIgE in and downregulated the expression of IL-1β, TNF-α, NF-κB, and WISP1 mRNA in the pulmonary. In addition, inhibited the expression of β-catenin, WISP1, and Wnt1 protein and upregulated the expression of glycogen synthase kinase-3beta (GSK-3β). Nebulized inhalation of can reduce airway remodeling during asthma.