Astragalin inhibits allergic asthma through modulating oxidative stress‐responsive MAPK signaling

Abstract

Allergic asthma is airway obstruction and chronic inflammation and is triggered by inhaled allergens such as dust mite allergen and pollen. Since inflammation is often associated with an increased generation of reactive oxygen species (ROS), and the biochemical environment in the asthmatic airways is favorable for ROS‐mediated reactions, it can be assumed that oxidative stress is a mechanistically‐imperative factor in asthma. Astragalin (kampferol‐3‐O‐glucopyranoside), a flavonoid with anti‐cancer, antimicrobial properties, has been isolated from tea seeds. This study elucidated whether oxidative stress activated allergic asthmatic responses in airway epithelial BEAS‐2B cells, which was suppressed by treating 1–20 μM astragalin. When airway epithelial cells were exposed to 2 μg/ml LPS, nontoxic astragalin at 1–20 μM suppressed LPS‐induced ROS production, evidenced by fluorescent DCFH‐DA staining. Astragalin attenuated LPS‐enhanced expression of PKCβ2 and p22phox and H2O2‐upregulated phosphorylation of JNK and p38 rapidly within 30 min. In contrast, the phosphorylation of Akt and ERK increased due to astragalin treatment. Additionally, astragalin attenuated LPS‐ or H2O2‐induced eotaxin‐1 protein expression of epithelial cells. Therefore, dietary astragalin can be effective in ameliorating allergic airway diseases through modulating oxidative stress‐responsive MAPK signaling pathway.