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Topical application of silymarin reduces chemical‐induced irritant contact dermatitis in BALB/c mice
Author(s) -
Kang Jong Soon,
Han SangBae,
Lee Kiho,
Park SongKyu,
Kim Hwan Mook
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.663
Subject(s) - hacat , croton oil , irritant contact dermatitis , chemokine , pharmacology , chemistry , tumor necrosis factor alpha , keratinocyte , cell adhesion molecule , proinflammatory cytokine , inflammation , contact dermatitis , immunology , medicine , biochemistry , in vitro , allergy
In the present study, we report that topical application of silymarin reduces chemical‐induced irritant contact dermatitis in mice. Topical application of 2,4‐dinitrochlorobenzene (DNCB) induced an ear swelling in BALB/c mice and silymarin suppressed DNCB‐induced increase in ear thickness. Prophylactic and therapeutic application of silymarin showed similar effect on DNCB‐induced increase in ear thickness and skin water content. In addition, phobor ester‐ or croton oil‐induced increase in ear thickness was also inhibited by silymarin treatment. Silymarin also blocked neutrophil accumulation into the ear induced by these irritants. Further study demonstrated that DNCB‐induced expression of tumor necrosis factor‐α (TNF‐α), KC and adhesion molecules in mouse ear was suppressed by silymarin. Moreover, TNF‐α‐induced expression of cytokines, such as TNF‐α and IL‐1β, and a chemokine, IL‐8, were suppressed by silymarin treatment in human keratinocyte cell line, HaCaT. Silymarin also blocked TNF‐α‐ and DNCB‐induced NF‐κB activation in HaCaT. Collectively, these results demonstrate that topically applied silymarin inhibits chemical‐induced ICD in mice and this might be mediated, at least in part, by blocking NF‐κB activation and consequently inhibiting the expression of cytokines and adhesion molecules.