Asthma is characterized by chronic airway inflammation, which is the underlying cause of airway remodeling featured by goblet cell hyperplasia, subepithelial fibrosis, and proliferation of smooth muscle. Sevoflurane has been used to treat life-threatening asthma and our previous study shows that sevoflurane inhibits acute lung inflammation in ovalbumin (OVA)-induced allergic mice. However, the effect of sevoflurane on airway remodeling in the context of chronic airway inflammation and the underlying mechanism are still unknown. Here, female C57BL/6 mice were used to establish chronic airway inflammation model. Hematoxylin and eosin (H&E), periodic acid-Schiff (PAS), and Sirius red (SR) staining were used to evaluate airway remodeling. Protein levels of α-SMA, VEGF, and TGF-β1 in lung tissues were detected by western blotting analyses and immunohistochemistry staining. Results showed that inhalation of sevoflurane inhibited chronic airway inflammation including inflammatory cell infiltration and pro-inflammatory cytokine production in BALF of the OVA-challenged mice. Meanwhile, sevoflurane suppressed airway thickening, goblet cell hyperplasia, smooth muscle hyperplasia, collagen deposition, and fiber hyperplasia in the lung tissues of the mice with airway remodeling. Most notably, sevoflurane inhibited the OVA-induced expressions of VEGF and TGF-β1. These results suggested that sevoflurane effectively inhibits airway remodeling in mouse model of chronic airway inflammation, which may be due to the downregulation of VEGF and TGF-β1in lung tissues. Therefore, our results indicate a potential role of sevoflurane in inhibiting airway remodeling besides its known suppression effect on airway inflammation, and support the use of sevoflurane in treating severe asthma in ICU.
Keywords: airway inflammation; airway remodeling; asthma; sevoflurane.