Suppression of skin inflammation in keratinocytes and acute/chronic disease models by caffeic acid phenethyl ester
- Title
- Suppression of skin inflammation in keratinocytes and acute/chronic disease models by caffeic acid phenethyl ester
- Author
- 배옥남
- Keywords
- Caffeic acid phenethyl ester (CAPE); Skin inflammation; Nuclear factor kappa B (NF-kappa B); Atopic dermatitis; TPA-induced ear edema
- Issue Date
- 2015-04
- Publisher
- SPRINGER
- Citation
- ARCHIVES OF DERMATOLOGICAL RESEARCH, v. 307, NO. 3, Page. 219.0-227.0
- Abstract
- Skin inflammation plays a central role in the pathophysiology and symptoms of diverse chronic skin diseases including atopic dermatitis (AD). In this study, we examined if caffeic acid phenethyl ester (CAPE), a skin-permeable bioactive compound from propolis, was protective against skin inflammation using in vitro cell system and in vivo animal disease models. CAPE suppressed TNF-alpha-induced NF-kappa B activation and expression of inflammatory cytokines in human keratinocytes (HaCaT). The potency and efficacy of CAPE were superior to those of a non-phenethyl derivative, caffeic acid. Consistently, topical treatment of CAPE (0.5 %) attenuated 12-O-tetradecanoylphorbol-13-acetate(TPA)-induced skin inflammation on mouse ear as CAPE reduced ear swelling and histologic inflammation scores. CAPE suppressed increased expression of pro-inflammatory molecules such as TNF-alpha, cyclooxygenase-2 and inducible NO synthase in TPA-stimulated skin. TPA-induced phosphorylation of I kappa B and ERK was blocked by CAPE suggesting that protective effects of CAPE on skin inflammation is attributed to inhibition of NF-kappa B activation. Most importantly, in an oxazolone-induced chronic dermatitis model, topical application of CAPE (0.5 and 1 %) was effective in alleviating AD-like symptoms such as increases of trans-epidermal water loss, skin thickening and serum IgE as well as histologic inflammation assessment. Collectively, our results propose CAPE as a promising candidate for a novel topical drug for skin inflammatory diseases.
- URI
- https://link.springer.com/article/10.1007%2Fs00403-014-1529-8https://repository.hanyang.ac.kr/handle/20.500.11754/182367
- ISSN
- 0340-3696;1432-069X
- DOI
- 10.1007/s00403-014-1529-8
- Appears in Collections:
- COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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