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Yao Xue Xue Bao ; 42(10): 1050-3, 2007 Oct.
Article in Chinese | MEDLINE | ID: mdl-18229610

ABSTRACT

This study is to observe the inhibition of etoposide on allergic contact dermatitis (ACD) and explore its possible mechanism of action. Dinitrofluorobenzene was used to induce the allergic contact dermatitis in mouse ear. Three groups of animals were orally administrated with different doses of VP-16 (5, 10, and 20 mg x kg(-1)), separately, for six days. The degree of skin inflammatory reaction was observed by optical microscope. Expression of intercellular adhesion molecule (ICAM-1) was detected by immunohistochemical staining. Radioimmunoassay was applied to measure the serum level of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10). VP-16 significantly decreased inflammatory cell infiltration and the degree of infiltration reaction, and decreased the level of TNF-a in serum and the expression of ICAM-l in skin. VP-16 can significantly inhibit allergic contact dermatitis induced by DNFB. This therapeutic effect of VP-16 on murine ACD may be due to inhibiting expression of some cytokines.


Subject(s)
Dermatitis, Allergic Contact/metabolism , Etoposide/pharmacology , Intercellular Adhesion Molecule-1/metabolism , Tumor Necrosis Factor-alpha/blood , Animals , Anti-Inflammatory Agents/pharmacology , Dermatitis, Allergic Contact/blood , Dermatitis, Allergic Contact/etiology , Dinitrofluorobenzene , Female , Interleukin-10/blood , Male , Mice , Random Allocation , Skin/metabolism
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