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Schizonepeta tenuifolia Inhibits the Development of Atopic Dermatitis in Mice
Author(s) -
Choi You Yeon,
Kim Mi Hye,
Kim JongHyun,
Jung HyukSang,
Sohn Youngjoo,
Choi Young Jin,
Hwang Man Ki,
Kim SungHoon,
Kim Jinju,
Yang Woong Mo
Publication year - 2013
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4833
Subject(s) - proinflammatory cytokine , dermis , atopic dermatitis , tumor necrosis factor alpha , downregulation and upregulation , medicine , protein kinase a , epidermis (zoology) , immunoglobulin e , interleukin , immunology , pharmacology , kinase , antibody , chemistry , inflammation , cytokine , pathology , biochemistry , anatomy , gene
Historically, Schizonepeta tenuifolia (ST) has been used for the treatment of skin disorders, such as allergic dermatitis, eczema, and inflammatory diseases. In this study, we examined whether ST inhibited 2,4‐dinitrochlorobenzene (DNCB)‐induced atopic dermatitis (AD) in BALB/c mice. In histopathological analyses of the epidermis and dermis, skin thickness was significantly increased in DNCB‐induced mice as compared with normal group. Treatment with ST inhibited this inflammatory change and markedly suppressed the secretion of immunoglobulin E, tumor necrosis factor α, and interleukin 6 levels in the serum of DNCB‐induced mice. In addition, ST treatment significantly restored the upregulation of proinflammatory factors, such as nuclear factor (NF)‐κB and mitogen‐activated protein kinase expression. Taken together, due to its ability to suppress inflammatory factors and upregulate proinflammatory factors, ST may be useful as a therapeutic treatment for AD. ST extract application decreased both epidermis and dermis thickness in DNCB‐induced mice. In serum, ST reduced immunoglobulin E, tumor necrosis factor, and interleukin 6 level. In addition, ST suppressed NF‐κB activation as well as the mitogen‐activated protein kinase activities. Copyright © 2012 John Wiley & Sons, Ltd.