Topical application of silymarin reduces chemical-induced irritant contact dermatitis in BALB/c mice

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dc.contributor.authorM H Han-
dc.contributor.authorWoon Kee Yoon-
dc.contributor.authorHyunju Lee-
dc.contributor.authorS B Han-
dc.contributor.authorKiho Lee-
dc.contributor.authorSong Kyu Park-
dc.contributor.authorK H Yang-
dc.contributor.authorHwan Mook Kim-
dc.contributor.authorJong Soon Kang-
dc.date.accessioned2017-04-19T09:08:21Z-
dc.date.available2017-04-19T09:08:21Z-
dc.date.issued2007-
dc.identifier.issn1567-5769-
dc.identifier.uri10.1016/j.intimp.2007.08.019ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/8134-
dc.description.abstractIrritant contact dermatitis (ICD) is a non-allergic local inflammatory reaction of a skin and one of the most frequent occupational health problems. Silymarin has been clinically used in Europe for a long time to treat liver diseases and also known to have anti-cancer and anti-inflammatory activities. In the present study, we report that topical application of silymarin reduces chemical-induced ICD. 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 tumor necrosis factor-α (TNF-α) expression in mouse ear was suppressed by silymarin. DNCB-induced expression of KC, one of the main attractors of neutrophil in mice, and adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and E-selectin in mouse ear were also inhibited 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.-
dc.publisherElsevier-
dc.titleTopical application of silymarin reduces chemical-induced irritant contact dermatitis in BALB/c mice-
dc.title.alternativeTopical application of silymarin reduces chemical-induced irritant contact dermatitis in BALB/c mice-
dc.typeArticle-
dc.citation.titleInternational Immunopharmacology-
dc.citation.number13-
dc.citation.endPage1658-
dc.citation.startPage1651-
dc.citation.volume7-
dc.contributor.affiliatedAuthorWoon Kee Yoon-
dc.contributor.affiliatedAuthorHyunju Lee-
dc.contributor.affiliatedAuthorKiho Lee-
dc.contributor.affiliatedAuthorSong Kyu Park-
dc.contributor.affiliatedAuthorHwan Mook Kim-
dc.contributor.affiliatedAuthorJong Soon Kang-
dc.contributor.alternativeName한미화-
dc.contributor.alternativeName윤원기-
dc.contributor.alternativeName이현주-
dc.contributor.alternativeName한상배-
dc.contributor.alternativeName이기호-
dc.contributor.alternativeName박성규-
dc.contributor.alternativeName양규환-
dc.contributor.alternativeName김환묵-
dc.contributor.alternativeName강종순-
dc.identifier.bibliographicCitationInternational Immunopharmacology, vol. 7, no. 13, pp. 1651-1658-
dc.identifier.doi10.1016/j.intimp.2007.08.019-
dc.subject.keywordadhesion molecules-
dc.subject.keywordirritant contact dermatitis-
dc.subject.keywordNF-κB-
dc.subject.keywordsilymarin-
dc.subject.keywordTNF-α-
dc.subject.localAdhesion molecule-
dc.subject.localadhesion molecule-
dc.subject.localadhesion molecules-
dc.subject.localirritant contact dermatitis-
dc.subject.localIrritant contact dermatitis-
dc.subject.localNFkappaB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNf-κb-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localNuclear factor kappaB-
dc.subject.localNuclear factor κB-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor-kappa B-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localNuclear factor-κB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-kB-
dc.subject.localNF-kappa B-
dc.subject.localNF-kappaB-
dc.subject.localNF-ΚB-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localnuclear factor kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localnuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localSilymarin-
dc.subject.localsilymarin-
dc.subject.localTNF-a-
dc.subject.localTNF-alpha-
dc.subject.localTNF-α-
dc.subject.localTNFa-
dc.subject.localTNFα-
dc.subject.localTnf-α-
dc.subject.localTumor necrosis fa tor-α-
dc.subject.localTumor necrosis factor (TNF)-α-
dc.subject.localTumor necrosis factor alpha-
dc.subject.localTumor necrosis factor-alpha-
dc.subject.localTumor necrosis factor-α-
dc.subject.localtumor necrosis factor-alpha-
dc.subject.localtumor necrosis factor-α-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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