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Comparative Study
. 1997 Jun;21(3):357-69.
doi: 10.1023/a:1027358102096.

Effect of topically applied cyclosporin A on arachidonic acid (AA)- and tetradecanoylphorbol acetate (TPA)-induced dermal inflammation in mouse ear

V Puigneró  1 , J Queralt
Affiliations
Comparative Study

Effect of topically applied cyclosporin A on arachidonic acid (AA)- and tetradecanoylphorbol acetate (TPA)-induced dermal inflammation in mouse ear

V Puigneró et al. Inflammation. 1997 Jun.

Abstract

Topical cyclosporin A (CsA) was compared with dexamethasone, indomethacin and phenidone in edema, increases in vascular permeability, eicosanoids and cell-influx induced by arachidonic acid (AA) and tetradecanoylphorbol acetate (TPA) in mouse ears. CsA ED(50) on AA-edema (7.7 micrograms/ear) was similar to dexamethasone and lower than indomethacin and phenidone. CsA ED(50) in TPA edema (21 micrograms/ear) was higher than dexamethasone and lower than indomethacin or phenidone. All drugs equally reduce the AA-induced increase in vascular permeability, but CsA and dexamethasone had more activity on TPA. AA-increase in vascular 6-keto-PGF1 alpha was reduced by dexamethasone, indomethacin and phenidone but not by CsA; only phenidone reduced LTB4. TPA-increase in 6-keto-PGF1 alpha was reduced 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 similar reduction in neutrophil influx. CsA was shown to be a good topical anti-inflammatory drug.

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