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Anti-inflammatory effect of bee venom in phthalic anhydride-induced atopic dermatitis animal model

Authors
Lee, Yu JinOh, Myung JinLee, Dong HunLee, Yong SunLee, JiinKim, Deok-HyunChoi, Cheol-HoonSong, Min JongSong, Ho SuebHong, Jin Tae
Issue Date
Feb-2020
Publisher
SPRINGER BASEL AG
Keywords
Bee venom; Nf-kappa B; Cytokines; MAP kinase; IgE
Citation
INFLAMMOPHARMACOLOGY, v.28, no.1, pp.253 - 263
Journal Title
INFLAMMOPHARMACOLOGY
Volume
28
Number
1
Start Page
253
End Page
263
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/17845
DOI
10.1007/s10787-019-00646-w
ISSN
0925-4692
Abstract
Globally, many people have been affected with atopic dermatitis (AD), a chronic inflammatory skin disease. AD is associated with multiple factors such as genetic, inflammatory, and immune factors. Bee venom (BV) is now widely used for the treatment of several inflammatory diseases. However, its effect on 5% phthalic anhydride (PA)-induced AD has not been reported yet. We investigated the anti-inflammatory and anti-AD effects of BV in a PA-induced animal model of AD. Balb/c mice were treated with topical application of 5% PA to the dorsal skin and ears for induction of AD. After 24 h, BV was applied on the back and ear skin of the mice three times a week for 4 weeks. BV treatment significantly reduced the PA-induced AD clinical score, back and ear epidermal thickness, as well as IgE level and infiltration of immune cells in the skin tissues compared to those of control mice. The levels of inflammatory cytokines in the serum were significantly decreased in BV-treated group compared to PA-treated group. In addition, BV inhibited the expression of iNOS and COX-2 as well as the activation of mitogen-activated protein kinase (MAPK) and NF-& x4a1;B induced by PA in the skin tissues. We also found that BV abrogated the lipopolysaccharide or TNF-alpha/IFN-gamma-induced NO production, expression of iNOS and COX-2, as well as MAPK and NF-& x4a1;B signaling pathway in RAW 264.7 and HaCaT cells. These results suggest that BV may be a potential therapeutic macromolecule for the treatment of AD.
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