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Suppression of Th2-driven, allergen-induced airway inflammation by sauchinone
- Suppression of Th2-driven, allergen-induced airway inflammation by sauchinone
- Min, Hyun Jung; Won, Hee Yeon; Kim, Young Choong; Sung, Sang Hyun; Byun, Mi Ran; Hwang, Jun-Ha; Hong, Jeong-Ho; Hwang, Eun Sook
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS vol. 385, no. 2, pp. 204 - 209
- Sauchinone; Allergen-induced airway inflammation; GATA-3; Th2 cell development; Airway inflammatory diseases
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- SCIE; SCOPUS
- Document Type
- Sauchinone, a lignan compound isolated from the root of saururus chinensis, has been recently demonstrated to exhibit anti-inflammatory, activity via the Suppression of NF-kB p65 activity in vitro. In an effort to evaluate the in vivo anti-inflammatory function of sauchinone, we have evaluated the effects of sauchinone on allergen-induced airway inflammation using a murine model of allergic asthma. We observed that marked eosinophilic and lymphocyte infiltration in the BAL fluid were suppressed to a significant degree by sauchinone, and that mucus-secreting goblet cell hyperplasia and collagen deposition in the airways were also ameliorated by administration of sauchinone treatment. Moreover, gene expression of the inflammatory cytokines, IL-13, and IL-5 and eotaxin in the lung, and IL-5 in the draining lymph node were significantly decreased in sauchinone-treated mice. We demonstrated that sauchinone repressed Th2 cell development in vitro and IL-4 production by Th2 cells, and also inhibited GATA-3-mediated IL-5 promoter activity in a close-dependent manner. Collectively, sauchinone ameliorated allergen-induced airway inflammation, in part, by repressing GATA-3 activity for Th2 cell development, indicating the possible therapeutic potential of sauchinone in airway inflammatory diseases including allergic asthma and rhinitis. (C) 2009 Elsevier Inc. All rights reserved.
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