Atopic dermatitis (AD) is a common chronic inflammatory
skin disease associated with various factors, including immunological abnormalities and exposure to
allergens.
Astaxanthin (AST) is a xanthophyll
carotenoid that has recently been demonstrated to have anti-inflammatory effects and to regulate the expression of inflammatory
cytokines. Thus, we investigated whether AST could improve the
dermatitis and
pruritus in a murine model of AD using NC/Nga mice. In addition to a behavioral evaluation, the effects of AST on the AD were determined by the clinical skin severity score, serum
IgE level, histological analyses of skin, and by reverse transcription-PCR and Western blotting analyses for the expression of
inflammation-related factors. AST (100 mg/kg) or vehicle (
olive oil) was orally administered once day and three times a week for 26 days. When compared with vehicle-treated group, the administration of AST significantly reduced the clinical skin severity score. In addition, the spontaneous scratching in AD model mice was reduced by AST administration. Moreover, the serum
IgE level was markedly decreased by the
oral administration of AST compared to that in vehicle-treated mice. The number of eosinophils, total and degranulated mast cells all significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. The
mRNA and
protein levels of eotaxin, MIF,
IL-4,
IL-5 and
L-histidine decarboxylase were significantly decreased in the skin of AST-treated mice compared with vehicle-treated mice. These results suggest that AST improves the
dermatitis and
pruritus in AD via the regulation of the inflammatory effects and the expression of inflammatory
cytokines.