NF‐κB is involved in inhibition of lipoxin A4 on dermal inflammation and hyperplasia induced by mezerein

Please cite this paper as: NF‐κB is involved in inhibition of lipoxin A₄ on dermal inflammation and hyperplasia induced by mezerein. Experimental Dermatology 2010; 19 : e286–e288. Abstract: The mechanisms by which lipoxin A₄ (LXA₄) inhibit skin inflammation remain unclear. In the present studies, the ear inflammatory model was induced by topical application of mezerein. Treatment of the mouse ear with LXA₄ exhibited the inhibitory effects on oedema, neutrophil infiltration, vascular permeability, expressions of interleukin (IL)‐1, IL‐6 and IL‐8 mRNA, DNA‐binding activity of nuclear factor‐κB (NF‐κB), and on dermal hyperplasia. NF‐κB reporter activities and nuclear translocations of NF‐κB p65 in cultured keratinocytes stimulated by mezerein were inhibited by pretreatment of the cells with LXA₄. LXA₄ reduced degradation, but not phosphorylation of IκBα in cultured keratinocytes stimulated by mezerein, suggesting that LXA₄‐attenuated IκBα degradation may restore the mezerein‐blocked inhibitory effects of IκB on nuclear translocation and DNA‐binding activity of NF‐κB. Our results demonstrated that LXA₄ displays the anti‐inflammatory and anti‐proliferative role on ear inflammatory model induced by mezerein and these effects were related with downregulation of DNA‐binding activity of NF‐κB.