title: α-Lipoic acid suppresses the development of DNFB-induced atopic dermatitis-like symptoms in NC/Nga mice.
abstract: 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.
authors.affiliation: Department of Microbiology (BK21), College of Medicine, Kyung Hee University, Seoul, Korea.
authors.forename: Gun-Dong
authors.initials: GD
authors.lastname: Kim
authors.forename: Tae-Ho
authors.initials: TH
authors.lastname: Kim
authors.forename: An-Hee
authors.initials: AH
authors.lastname: Jang
authors.forename: Hyun-Jong
authors.initials: HJ
authors.lastname: Ahn
authors.forename: Yong Seek
authors.initials: YS
authors.lastname: Park
authors.forename: Cheung-Seog
authors.initials: CS
authors.lastname: Park
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D049109:Cell Proliferation / Q000187:drug effects; D003876:Dermatitis, Atopic / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism; D004139:Dinitrofluorobenzene / Q000009:adverse effects*; D004195:Disease Models, Animal; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008063:Thioctic Acid / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D015847:Interleukin-4; D007073:Immunoglobulin E; D008063:Thioctic Acid; D007371:Interferon-gamma; D004139:Dinitrofluorobenzene