title: Vitamin E improves biochemical indices associated with symptoms of atopic dermatitis-like inflammation in NC/Nga mice.
abstract: We aimed to define whether vitamin E improves biochemical indices associated with symptoms of atopic dermatitis-like inflammation in NC/Nga mice. After picryl chloride (PC) application to their backs, changes in the content of thiobarbituric acid reactive substances (TBARS) and vitamin E, as well as the activity of antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and catalase) were analyzed in the serum and skin of NC/Nga mice during a symptomatic cycle. The levels of inflammatory factors were also assessed, including IgE, cyclooxigenase-2 (COX-2), tumor necrosis factor (TNF-α) and nuclear factor-κB (NF-κB). When allergic dermatitis was induced by the application of PC to the skin of the mice, skin inflammation appeared 2 wk after PC application, with the peak severity of inflammation observed 5 wk after PC application. Subsequently, the animals recovered from the inflammation by 9 wk after PC application. The TBARS content in the skin and serum increased markedly when the symptoms were the most severe, and decreased to levels near those in control mice by 9 wk after PC application. The activities of SOD and GSHPx in the skin and serum were also positively correlated with symptomatic changes; however, no change in catalase activity was observed 5 wk after PC application. Conversely, vitamin E content decreased at the stage of peak severity. The levels of all inflammatory factors analyzed in this study were altered in a manner similar to other indices. Additionally, vitamin E treatment markedly inhibited these PC-induced alterations. On the basis of these results, it is expected that the observed alterations in biochemical indices, which reflect the symptomatic cycle, may be applicable to objective diagnosis and treatment for atopic dermatitis, and that vitamin E may improve the symptoms of AD.
authors.affiliation: Division of Biological Chemistry, Shibaura Institute of Technology, Kohtoh-ku, Tokyo, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Hayashi
authors.forename: Hotaka
authors.initials: H
authors.lastname: Sugaya
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ohkoshi
authors.forename: Kaori
authors.initials: K
authors.lastname: Sekizawa
authors.forename: Hirokatsu
authors.initials: H
authors.lastname: Takatsu
authors.forename: Tadashi
authors.initials: T
authors.lastname: Shinkai
authors.forename: Shiro
authors.initials: S
authors.lastname: Urano
mesh_terms: D000818:Animals; D002374:Catalase / Q000032:analysis / Q000097:blood; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000097:blood; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology*; D005979:Glutathione Peroxidase / Q000032:analysis / Q000097:blood; D007073:Immunoglobulin E / Q000032:analysis / Q000097:blood; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000032:analysis / Q000097:blood; D018384:Oxidative Stress; D010853:Picryl Chloride / Q000008:administration & dosage; D012867:Skin / Q000737:chemistry / Q000473:pathology; D013482:Superoxide Dismutase / Q000032:analysis / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000097:blood; D014810:Vitamin E / Q000008:administration & dosage* / Q000032:analysis / Q000097:blood
chemical_list: D016328:NF-kappa B; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D014810:Vitamin E; D007073:Immunoglobulin E; D002374:Catalase; D005979:Glutathione Peroxidase; D051546:Cyclooxygenase 2; D013482:Superoxide Dismutase; D010853:Picryl Chloride