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[6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo

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dc.contributor.authorKim, Jin-Kyoung-
dc.contributor.authorKim, Younghwa-
dc.contributor.authorNa, Kwang-Min-
dc.contributor.authorSurh, Young-Joon-
dc.contributor.authorKim, Tae-Yoon-
dc.date.accessioned2021-01-31T10:14:08Z-
dc.date.available2021-01-31T10:14:08Z-
dc.date.created2017-11-15-
dc.date.issued2007-
dc.identifier.citationFree Radical Research, Vol.41 No.5, pp.603-614-
dc.identifier.issn1071-5762-
dc.identifier.other3558-
dc.identifier.urihttps://hdl.handle.net/10371/172748-
dc.description.abstract[6]-Gingerol, a naturally occurring plant phenol, is one of the major components of fresh ginger (Zingiber officinale Roscoe, Zingiberaceae) and has diverse pharmacologic effects. Here, we describe its novel anti-oxidant, anti-apoptotic, and anti-inflammatory activities in vitro and in vivo. In vitro, pre-treatment with [6]-gingerol reduced UVB-induced intracellular reactive oxygen species levels, activation of caspase-3, -8, -9, and Fas expression. It also reduced UVB-induced expression and transactivation of COX-2. Translocation of NF-kappa B from cytosol to nucleus in HaCaT cells was inhibited by [6]-gingerol via suppression of I kappa B alpha phosphorylation (ser-32). Examination by EMSAs and immunohistochemistry showed that topical application of [6]-gingerol (30 mM) prior to UVB irradiation (5 kJ/m(2)) of hairless mice, also inhibited the induction of COX-2 mRNA and protein, as well as NF-kappa B translocation. These results suggest that [6]-gingerol could be an effective therapeutic agent providing protection against UVB-induced skin disorders.-
dc.language영어-
dc.publisherTaylor & Francis-
dc.title[6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1080/10715760701209896-
dc.citation.journaltitleFree Radical Research-
dc.identifier.wosid000245589100011-
dc.identifier.scopusid2-s2.0-34047135039-
dc.citation.endpage614-
dc.citation.number5-
dc.citation.startpage603-
dc.citation.volume41-
dc.identifier.sci000245589100011-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorSurh, Young-Joon-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusESTER-INDUCED EXPRESSION-
dc.subject.keywordPlusHUMAN SKIN FIBROBLASTS-
dc.subject.keywordPlusGROWTH-FACTOR RECEPTOR-
dc.subject.keywordPlusP38 MAP KINASE-
dc.subject.keywordPlusHUMAN KERATINOCYTES-
dc.subject.keywordPlusMOUSE SKIN-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusCYCLOOXYGENASE-2 EXPRESSION-
dc.subject.keywordPlusORNITHINE-DECARBOXYLASE-
dc.subject.keywordAuthorUVB-
dc.subject.keywordAuthor[6]-gingerol-
dc.subject.keywordAuthorROS-
dc.subject.keywordAuthorcyclooxygenase-2-
dc.subject.keywordAuthorNF-kappa B-
dc.subject.keywordAuthorcaspase-
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  • College of Pharmacy
  • Department of Pharmacy
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