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dc.contributor.authorKim, Min-Jin-
dc.contributor.authorKim, Se-Jae-
dc.contributor.authorKim, Sang Suk-
dc.contributor.authorLee, Nam Ho-
dc.contributor.authorHyun, Chang-Gu-
dc.date.accessioned2014-05-14T12:39:03Z-
dc.date.available2014-05-14T12:39:03Z-
dc.date.issued2014-02-17-
dc.identifier.issn1611-2156-
dc.identifier.urihttp://hdl.handle.net/2003/33130-
dc.identifier.urihttp://dx.doi.org/10.17877/DE290R-13720-
dc.description.abstractHypochoeris radicata, an invasive plant species, is a large and growing threat to ecosystem integrity on Jeju Island, a UNESCO World Heritage site. Therefore, research into the utilization of H. radicata is important and urgently required in order to solve this invasive plant problem in Jeju Island. The broader aim of our research is to elucidate the biological activities of H. radicata, which would facilitate the conversion of this invasive species into high value added products. The present study was undertaken to identify the pharmacological effects of H. radicata flower on the production of inflammatory mediators in macrophages. The results indicate that the ethyl acetate fraction of H. radicata extract (HRF-EA) inhibited the production of pro-inflammatory molecules such as NO, iNOS, PGE2, and COX-2, and cytokines such as TNF-α, IL-1β, and IL-6 in LPS-stimulated RAW 264.7 cells. Furthermore, the phosphorylation of MAPKs such as p38, ERK, and JNK was suppressed by HRF-EA in a concentration-dependent manner. In addition, through HPLC and UPLC fingerprinting, luteolins were also identified and quantified as extract constituents. On the basis of these results, we suggest that H. radicata may be considered possible anti-inflammatory candidates for pharmaceutical and/or cosmetic applications.en
dc.language.isoen-
dc.relation.ispartofseriesEXCLI Journal ; Vol. 13, 2014en
dc.subjectHypochoeris radicataen
dc.subjectalien plant invaderen
dc.subjectinflammationen
dc.subjectmitogen-activated protein kinases (MAPKs)en
dc.subject.ddc610-
dc.titleHypochoeris radicata attenuates LPS-induced inflammation by suppressing P38, ERK, and JNK phosphorylation in Raw 264.7 macrophagesen
dc.typeText-
dc.type.publicationtypearticle-
dcterms.accessRightsopen access-
eldorado.dnb.zdberstkatid2132560-1-
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