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

Oleh:

Gong, Ju-Hyun ; Shin, Daekeun ; Han, Seon-Young ; Kim, Jung-Lye ; Kang, Young-Hee

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 142 no. 01 (Jan. 2012), page 47-56.
Topik: Nutrition and Disease

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2012.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

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, 1–20 µmol/L kaempferol dose-dependently attenuated TNFa-induced expression of epithelial intracellular cell adhesion molecule-1 and eosinophil integrin ß2, thus encumbering the eosinophil-airway epithelium interaction. Kaempferol blunted TNFa-induced airway inflammation by attenuating monocyte chemoattractant protein-1 transcription, possibly by disturbing NF-?B 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-?B 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-?B signaling.

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