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Oral Administration of Herbal Mixture Extract Inhibits 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis in BALB/c Mice

Authors
Kim, Soon ReChoi, Han-SeokSeo, Hye SookKu, Jin MoHong, Se HyangYoo, Hye HyunShin, Yong CheolKo, Seong-Gyu
Issue Date
Jul-2014
Publisher
Hindawi Publishing Corporation
Keywords
REHMANNIA-GLUTINOSA; ADHESION MOLECULE-1; SKIN-LESIONS; PLATYPHYLLA VAR. JAPONICA; INFLAMMATION; IGE; MAST-CELLS; DISEASE; NECROSIS-FACTOR-ALPHA; NC/NGA MICE
Citation
Mediators of Inflammation, v.2014, pp.1 - 11
Indexed
SCIE
SCOPUS
Journal Title
Mediators of Inflammation
Volume
2014
Start Page
1
End Page
11
URI
https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/25901
DOI
10.1155/2014/319438
ISSN
0962-9351
Abstract
CP001 is four traditional herbal medicine mixtures with anti-inflammatory properties. In this study, we investigated the effect of oral administration of CP001 ethanol extract on the 2,4-dinitrochlorobenzene- (DNCB-) induced AD mouse models. For that purpose, we observed the effects of oral administration of CP001 on skin inflammatory cell infiltration, skin mast cells, production of serum IgE, and expression of Th2 cytokine mRNA in the AD skin lesions of DNCB treated BALB/c mice. Histological analyses demonstrated that CP001 decreased dermis and epidermis thickening as well as dermal infiltration induced by inflammatory cells. In addition, CP001 decreased mast cell infiltration in count as well as dermal infiltration induced by inflammatory cells. In the skin lesions, mRNA expression of interleukin- (IL-) 4 and IL-13 was inhibited by CP001. CP001 also reduced the production of IgE level in mouse plasma. In addition, we investigated the effect of CP001 on the inflammatory allergic reaction using human mast cells (HMC-1). In HMC-1, cytokine production and mRNA levels of IL-4, IL-13, IL-6, and IL-8 were suppressed by CP001. Taken together, our results showed that oral administration of CP001 exerts beneficial effects in AD symptoms, suggesting that CP001 might be a useful candidate for the treatment of AD.
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