[Effect of etoposide on allergic contact dermatitis induced by dinitrofluorobenzene and its action mechanism in mice].
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.
Xie
Qing
Q
Department of Pharmacy, Qilu Hospital, China.
Yan
Hui-lan
HL
Li
Ying-quan
YQ
Wang
Jin
J
Wang
Ju-ying
JY
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D017449:Dermatitis, Allergic Contact / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D004139:Dinitrofluorobenzene; D005047:Etoposide / Q000494:pharmacology*; D005260:Female; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D051379:Mice; D011897:Random Allocation; D012867:Skin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
D000893:Anti-Inflammatory Agents; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; D005047:Etoposide; D004139:Dinitrofluorobenzene