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α‐Lipoic acid suppresses the development of DNFB‐induced atopic dermatitis‐like symptoms in NC/Nga mice
Author(s) -
Kim GunDong,
Kim TaeHo,
Jang AnHee,
Ahn HyunJong,
Park Yong Seek,
Park CheungSeog
Publication year - 2011
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2010.01165.x
Subject(s) - atopic dermatitis , immunoglobulin e , lipoic acid , immunology , reactive oxygen species , chemistry , interleukin , cytokine , pharmacology , interferon , proinflammatory cytokine , inflammation , medicine , biochemistry , antioxidant , antibody
Atopic dermatitis (AD) is a common skin disease that has complex pathogenic mechanisms. Under specific pathogen‐free conditions, repeated epicutaneous treatment of 2‐4‐dinitrofluorobenzene (DNFB) evokes AD‐like clinical symptoms in NC/Nga mice. α‐Lipoic acid (α‐LA; 1, 2‐dithiolane‐3‐pentanoic acid) is a dietary component that is synthesized in bacteria, yeast, plants, and mammals. α‐LA and its reduced form, dihydrolipoic acid, are powerful antioxidants that have many physiological functions, including free radical scavenging of reactive oxygen species, generation of cellular antioxidants, chelation of metal ions, and inflammatory suppression. In this study, we investigated whether α‐LA suppresses AD‐like skin lesions induced by repeated DNFB application in NC/Nga mice. α‐LA significantly suppressed production of interferon (IFN)‐γ and interleukin (IL)‐4 by activated CD4 + T cells. We found that the oral administration of α‐LA reduced AD‐like clinical symptoms and inhibited increases of epidermal thickness in DNFB‐induced AD‐like skin lesions of NC/Nga mice. Furthermore, total serum IgE levels were dramatically reduced by topical α‐LA treatment. Our findings suggest that oral administration of α‐LA suppresses the development of AD in DNFB‐treated NC/Nga mice and reduces IFN‐γ and IL‐4 production from activated CD4 + T cells as well as total serum IgE levels.