Suppression of skin inflammation in keratinocytes and
acute/chronic disease models by caffeic acid phenethyl ester
Date: 12 Dec 2014
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-α-induced NF-κB 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-α,
cyclooxygenase-2 and inducible NO synthase in TPA-stimulated skin. TPA-induced
phosphorylation of IκB and ERK was blocked by CAPE suggesting that protective
effects of CAPE on skin inflammation is attributed to inhibition of NF-κB
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.
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