期刊
JOURNAL OF NUTRITION
卷 142, 期 1, 页码 47-56出版社
OXFORD UNIV PRESS
DOI: 10.3945/jn.111.150748
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资金
- National Research Foundation of Korea
- Korean Government [2009-0072534]
- Korea Research Foundation
- Korean Government (MEST)
- Medical and Bio-Materials Research Center
- National Research Foundation of Korea [2009-0072534] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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,mu mol/L, suppressed LPS-induced eotaxin-1 protein expression that may be mediated, likely via Janus kinase 2 (JAK2) JAK2 signaling. Additionally, 1-20 mu mol/L kaempferol dose-dependently attenuated TNF alpha-induced expression of epithelial intracellular cell adhesion molecule-1 and eosinophil integrin beta 2, thus encumbering the eosinophil-airway epithelium interaction. Kaempferol blunted TNF alpha-induced airway inflammation by attenuating monocyte chemoattractant protein-1 transcription, possibly by disturbing NF-kappa 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-kappa 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-kappa B signaling. J. Nutr. 142: 47-56,2012.
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