EFFECT OF TOPICALLY APPLIED CYCLOSPORINE-A ON ARACHIDONIC-ACID (AA)-INDUCED AND TETRADECANOYLPHORBOL ACETATE (TPA)-INDUCED DERMAL INFLAMMATION IN MOUSE EAR

Topical cyclosporin A (CsA) was compared with dexamethasone, indometha cin and phenidone in edema, increases in vascular permeability, eicosa noids and cell-influx induced by arachidonic acid (AA) and tetradecano ylphorbol acetate (TPA) in mouse ears. CsA ED50 on AA-edema (7.7 mu g/ ear) was similar to dexamethasone and lower than indomethacin and phen idone. CsA ED50 in TPA edema (21 mu g/ear) was higher than dexamethaso ne and lower than indomethacin or phenidone. All drugs equally reduce the AA-induced increase in vascular permeability, but CsA and dexameth asone had more activity on TPA. AA-increase in 6-keto-PGF(1 alpha) was reduced by dexamethasone, indomethacin and phenidone but not by CsA; only phenidone reduced LTB4. TPA-increase in 6-keto-PGF(1 alpha) was r educed by CsA and indomethacin while CsA, dexamethasone and phenidone decreased LTB4. CsA, indomethacin and phenidone, but not dexamethasone , suppressed AA-neutrophil influx. In TPA-ears all drugs produced simi lar reduction in neutrophil influx. CsA was shown to be a good topical anti-inflammatory drug.