DC Field | Value | Language |
---|---|---|
dc.contributor.author | M H Han | - |
dc.contributor.author | Woon Kee Yoon | - |
dc.contributor.author | Hyunju Lee | - |
dc.contributor.author | S B Han | - |
dc.contributor.author | Kiho Lee | - |
dc.contributor.author | Song Kyu Park | - |
dc.contributor.author | K H Yang | - |
dc.contributor.author | Hwan Mook Kim | - |
dc.contributor.author | Jong Soon Kang | - |
dc.date.accessioned | 2017-04-19T09:08:21Z | - |
dc.date.available | 2017-04-19T09:08:21Z | - |
dc.date.issued | 2007 | - |
dc.identifier.issn | 1567-5769 | - |
dc.identifier.uri | 10.1016/j.intimp.2007.08.019 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/8134 | - |
dc.description.abstract | Irritant 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.publisher | Elsevier | - |
dc.title | Topical application of silymarin reduces chemical-induced irritant contact dermatitis in BALB/c mice | - |
dc.title.alternative | Topical application of silymarin reduces chemical-induced irritant contact dermatitis in BALB/c mice | - |
dc.type | Article | - |
dc.citation.title | International Immunopharmacology | - |
dc.citation.number | 13 | - |
dc.citation.endPage | 1658 | - |
dc.citation.startPage | 1651 | - |
dc.citation.volume | 7 | - |
dc.contributor.affiliatedAuthor | Woon Kee Yoon | - |
dc.contributor.affiliatedAuthor | Hyunju Lee | - |
dc.contributor.affiliatedAuthor | Kiho Lee | - |
dc.contributor.affiliatedAuthor | Song Kyu Park | - |
dc.contributor.affiliatedAuthor | Hwan Mook Kim | - |
dc.contributor.affiliatedAuthor | Jong Soon Kang | - |
dc.contributor.alternativeName | 한미화 | - |
dc.contributor.alternativeName | 윤원기 | - |
dc.contributor.alternativeName | 이현주 | - |
dc.contributor.alternativeName | 한상배 | - |
dc.contributor.alternativeName | 이기호 | - |
dc.contributor.alternativeName | 박성규 | - |
dc.contributor.alternativeName | 양규환 | - |
dc.contributor.alternativeName | 김환묵 | - |
dc.contributor.alternativeName | 강종순 | - |
dc.identifier.bibliographicCitation | International Immunopharmacology, vol. 7, no. 13, pp. 1651-1658 | - |
dc.identifier.doi | 10.1016/j.intimp.2007.08.019 | - |
dc.subject.keyword | adhesion molecules | - |
dc.subject.keyword | irritant contact dermatitis | - |
dc.subject.keyword | NF-κB | - |
dc.subject.keyword | silymarin | - |
dc.subject.keyword | TNF-α | - |
dc.subject.local | Adhesion molecule | - |
dc.subject.local | adhesion molecule | - |
dc.subject.local | adhesion molecules | - |
dc.subject.local | irritant contact dermatitis | - |
dc.subject.local | Irritant contact dermatitis | - |
dc.subject.local | NFkappaB | - |
dc.subject.local | NFκB | - |
dc.subject.local | Nf-κB | - |
dc.subject.local | Nf-κb | - |
dc.subject.local | Nuclear factor (NF)-κB | - |
dc.subject.local | Nuclear factor kappa B | - |
dc.subject.local | Nuclear factor kappaB | - |
dc.subject.local | Nuclear factor κB | - |
dc.subject.local | Nuclear factor κB (NF-κB) | - |
dc.subject.local | Nuclear factor-kappa B | - |
dc.subject.local | Nuclear factor-kappa B (NF-κB) | - |
dc.subject.local | Nuclear factor-kappaB | - |
dc.subject.local | Nuclear factor-κB | - |
dc.subject.local | Nuclear factor-κb | - |
dc.subject.local | NF-kB | - |
dc.subject.local | NF-kappa B | - |
dc.subject.local | NF-kappaB | - |
dc.subject.local | NF-ΚB | - |
dc.subject.local | NF-κ B | - |
dc.subject.local | NF-κB | - |
dc.subject.local | NF-κB (nuclear factor kappa-B) | - |
dc.subject.local | nuclear factor kappa B | - |
dc.subject.local | nuclear factor κB | - |
dc.subject.local | nuclear factor-kappaB | - |
dc.subject.local | nuclear factor-kappaB (NF-κB) | - |
dc.subject.local | nuclear factor-κB | - |
dc.subject.local | nuclear factorκB | - |
dc.subject.local | Silymarin | - |
dc.subject.local | silymarin | - |
dc.subject.local | TNF-a | - |
dc.subject.local | TNF-alpha | - |
dc.subject.local | TNF-α | - |
dc.subject.local | TNFa | - |
dc.subject.local | TNFα | - |
dc.subject.local | Tnf-α | - |
dc.subject.local | Tumor necrosis fa tor-α | - |
dc.subject.local | Tumor necrosis factor (TNF)-α | - |
dc.subject.local | Tumor necrosis factor alpha | - |
dc.subject.local | Tumor necrosis factor-alpha | - |
dc.subject.local | Tumor necrosis factor-α | - |
dc.subject.local | tumor necrosis factor-alpha | - |
dc.subject.local | tumor necrosis factor-α | - |
dc.description.journalClass | Y | - |
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