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Protective Effects of Cyclooxygenase‐2 Inhibitors on Narrow‐band Ultraviolet B‐irradiated Epidermal Ia + Langerhans Cells and Thy‐1 + Dendritic Epidermal T Cells in Mice †
Author(s) -
Wu Yan,
Tai ChangLong,
Wei Huachen,
He Fang,
Wang Yakun,
Zhao Yuming,
Chen HongDuo
Publication year - 2008
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2007.00289.x
Subject(s) - cyclooxygenase , chemistry , irradiation , microbiology and biotechnology , biology , immunology , cancer research , pharmacology , enzyme , biochemistry , physics , nuclear physics
Abstract Cyclooxygenase (COX)‐2 inhibitors are known to be used as chemopreventative agents against certain malignancies. Thus far, there has been very limited information on whether COX‐2 inhibitors protect against chronic narrow‐band UVB (NB‐UVB)‐induced immunosuppression. The present study investigated the effect of nonselective and specific COX‐2 inhibitors, indomethacin and celecoxib, on epidermal Ia + Langerhans cells (LCs) and Thy‐1 + dendritic epidermal T cells (DETCs) in mice irradiated with NB‐UVB. Sixty female BALB/c mice were divided randomly into the control group (sham) and the experimental groups (irradiated with NB‐UVB for 17 weeks, further divided into five groups according to the diets containing different concentrations of either COX‐2 inhibitors). Alterations in the density and morphology of epidermal Ia + LCs and Thy‐1 + DETCs in mice were documented using fluorescence microscopy. Chronic NB‐UVB irradiation substantially decreased the density and altered the morphology of the epidermal Ia + LCs and Thy‐1 + DETCs in control mice. The dietary supplementation of both COX‐2 inhibitors displayed a dosage‐dependent protective effect on the murine dendritic cells irradiated by NB‐UVB. In conclusion, COX‐2 inhibitors protected against chronic NB–UVB‐induced density and morphologic changes in epidermal Ia + LCs and Thy‐1 + DETCs in mice.