Eupatilin, an activator of PPAR alpha, inhibits the development of oxazolone-induced atopic dermatitis symptoms in Balb/c mice

Authors
Jung, YujungKim, Jin-ChulPark, No-JuneBong, Sim-KyuLee, SullimLegal, HyunJin, Li TaiKim, Sang MooKim, Yong KeeKim, Su-Nam
Issue Date
2018-02-05
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.496, no.2, pp.508 - 514
Abstract
Eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone) is the main lipophilic flavonoid obtained from the Artemisia species. Eupatilin has been reported to have anti-apoptotic, anti-oxidative and anti-inflammatory activities. Previously, we found that eupatilin increases transcriptional activity and expression of peroxisome proliferator-activated receptor alpha (PPAR alpha) in a keratinocyte cell line and acts as an agonist of PPAR alpha. PPAR alpha agonists ameliorate atopic dermatitis (AD) and restore the skin barrier function. In this study, we confirmed that the effects of eupatilin improved AD-like symptoms in an oxazolone-induced AD-like mouse model. Furthermore, we found that eupatilin suppressed the levels of serum immunoglobulin E (IgE), interleukin-4 (IL-4), and AD involved cytokines, such as tumor necrosis factor alpha (TNF alpha), interferon-gamma (IFN-gamma), IL-1 beta, and thymic stromal lymphopoietin (TSLP), IL-33, IL-25 and increased the levels of filaggrin and loricrin in the oxazolone-induced AD-like mouse model. Taken together, our data suggest that eupatilin is a potential candidate for the treatment of AD. (C) 2018 Elsevier Inc. All rights reserved.
Keywords
THYMIC STROMAL LYMPHOPOIETIN; MAST-CELLS; EPIDERMAL-KERATINOCYTES; ALLERGIC INFLAMMATION; IN-VIVO; EXPRESSION; SKIN; TRANSCRIPTION; CYTOKINE; DIFFERENTIATION; THYMIC STROMAL LYMPHOPOIETIN; MAST-CELLS; EPIDERMAL-KERATINOCYTES; ALLERGIC INFLAMMATION; IN-VIVO; EXPRESSION; SKIN; TRANSCRIPTION; CYTOKINE; DIFFERENTIATION; Eupatilin; PPAR alpha; Atopic dermatitis; IL-4
ISSN
0006-291X
URI
https://pubs.kist.re.kr/handle/201004/121714
DOI
10.1016/j.bbrc.2018.01.098
Appears in Collections:
KIST Article > 2018
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