Astragalin attenuates allergic airway inflammation by modulating macrophage infiltration in asthmatic mice

Pulmonary fibrosis and destruction are likely to be the main contributors to pathophysiological lung dysfunction, which may be attributed to any subsequent development of emphysema. We recently reported that astragalin allayed oxidative stress‐associated pulmonary fibrosis through disturbing airway epithelial mesenchymal transition and epithelial autophagic stress. This study attempted to identify how airway inflammation and remodeling led to the failure of lung function and how astragalin affected airway and pulmonary remodeling in the progression of inflammatory lung diseases including asthma, emphysema and pulmonary fibrosis. We found that astragalin attenuated pro‐inflammatory responses through diminishing the MCP‐1 secretion and the ICAM‐1 expression in 20 μM H 2 O 2 ‐exposed airway epithelial BEAS‐2B cells. Oral administration of astragalin suppressed the induction of MCP‐1, CD11b(+) and F4/80(+) in OVA‐sensitized mouse airways and lungs. Additionally, mast cells were infiltrated in the airway epithelium in OVA‐challenged mice, and such infiltration was blocked by supplementing 20 mg/kg astragalin in sensitized‐mice. Our results demonstrated that astragalin may ameliorate pulmonary inflammation and remodeling by suppressing the production of several inflammatory mediators. Support or Funding Information This study was supported by Brain Korea 21 plus program by Ministry of Education of Korea (22A20130012421).