Kaempferol Suppresses Eosionphil Infiltration and Airway Inflammation in Airway Epithelial Cells and in Mice with Allergic Asthma ,

Abstract

The airway epithelium is thought to play an important role in the pathogenesis of asthma. Airway epithelial activation may contribute to inflammatory and airway-remodeling events characteristic of asthma. Kaempferol, a flavonoid with antioxidative and antitumor properties, has been studied as an antiinflammatory agent. However, little is known regarding its effects on allergic asthma. Human airway epithelial BEAS-2B cells and eosinophils were used to investigate the effects of kaempferol on endotoxin- or cytokine-associated airway inflammation. Kaempferol, nontoxic at 1–20 µmol/L, suppressed LPS-induced eotaxin-1 protein expression that may be mediated, likely via Janus kinase 2 (JAK2) JAK2 signaling. Additionally, 1–20µmol/L kaempferol dose-dependently attenuated TNFα-induced expression of epithelial intracellular cell adhesion molecule-1 and eosinophil integrin β2, thus encumbering the eosinophil-airway epithelium interaction. Kaempferol blunted TNFα-induced airway inflammation by attenuating monocyte chemoattractant protein-1 transcription, possibly by disturbing NF-кB signaling. This study further investigated antiallergic activity of kaempferol in BALB/c mice sensitized with ovalbumin (OVA) and challenged with a single dose of OVA. Oral administration of kaempferol attenuated OVA challenge–elevated expression of eotaxin-1 and eosinophil major basic protein via the blockade of NF-кB transactivation, thereby blunting eosinophil accumulation in airway and lung tissue. Therefore, dietary kaempferol is effective in ameliorating allergic and inflammatory airway diseases through disturbing NF-кB signaling.