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dc.contributor.authorLee, Geumho-
dc.contributor.authorChoi, Tae Won-
dc.contributor.authorKim, Chulwon-
dc.contributor.authorNam, Dongwoo-
dc.contributor.authorLee, Seok-Geun-
dc.contributor.authorJang, Hyeung-Jin-
dc.contributor.authorLee, Jun-Hee-
dc.contributor.authorUm, Jae-Young-
dc.contributor.authorJung, Sang Hoon-
dc.contributor.authorShim, Bum Sang-
dc.contributor.authorAhn, Kyoo Seok-
dc.contributor.authorAhn, Kwang Seok-
dc.date.accessioned2024-01-20T14:33:42Z-
dc.date.available2024-01-20T14:33:42Z-
dc.date.created2021-09-05-
dc.date.issued2012-06-
dc.identifier.issn0892-3973-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/129191-
dc.description.abstractReynoutria elliptica has been used in traditional Korean medicine to promote blood circulation, relieve pain, increase dieresis, and alleviate respiratory problems, through as yet undefined mechanisms. We set out to determine whether the anti-inflammatory effects of this plant are linked with its ability to suppress mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappa B) activation in lipopolysaccharide (LPS)-activated RAW 264.7 cells. We found for the first time that the hexane fraction of Reynoutria elliptica (HRE) significantly inhibited LPS-stimulated NO and PGE2 synthesis. This is due to the diminishing of the mRNA and protein expression of iNOS and COX-2, respectively. HRE also suppressed LPS-stimulated TNF-alpha secretion in a dose-dependent manner, which might be due to the suppression of LPS-induced MAPKs and NF-kappa B activation. Moreover, our HPLC data demonstrated that the major components of the HRE were bioactive compounds such as emodin-6-Glc, emodin, and physcion. Overall, our results indicate that Reynoutria elliptica could be provided as a potential candidate for anti-inflammation treatment.-
dc.languageEnglish-
dc.publisherINFORMA HEALTHCARE-
dc.subjectNITRIC-OXIDE SYNTHASE-
dc.subjectVASCULAR ENDOTHELIAL-CELLS-
dc.subjectTRANSCRIPTION FACTOR-
dc.subjectINTERFERON-GAMMA-
dc.subjectGENE-EXPRESSION-
dc.subjectP38 MAPK-
dc.subjectBACTERIAL LIPOPOLYSACCHARIDE-
dc.subjectDOWN-REGULATION-
dc.subjectPHORBOL ESTER-
dc.subjectEMODIN-
dc.titleAnti-inflammatory activities of Reynoutria elliptica through suppression of mitogen-activated protein kinases and nuclear factor-kappa B activation pathways-
dc.typeArticle-
dc.identifier.doi10.3109/08923973.2011.619195-
dc.description.journalClass1-
dc.identifier.bibliographicCitationIMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY, v.34, no.3, pp.454 - 464-
dc.citation.titleIMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY-
dc.citation.volume34-
dc.citation.number3-
dc.citation.startPage454-
dc.citation.endPage464-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000303830400014-
dc.identifier.scopusid2-s2.0-84860712887-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaToxicology-
dc.type.docTypeArticle-
dc.subject.keywordPlusNITRIC-OXIDE SYNTHASE-
dc.subject.keywordPlusVASCULAR ENDOTHELIAL-CELLS-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusINTERFERON-GAMMA-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusP38 MAPK-
dc.subject.keywordPlusBACTERIAL LIPOPOLYSACCHARIDE-
dc.subject.keywordPlusDOWN-REGULATION-
dc.subject.keywordPlusPHORBOL ESTER-
dc.subject.keywordPlusEMODIN-
dc.subject.keywordAuthorReynoutria elliptica-
dc.subject.keywordAuthorNF-kappa B-
dc.subject.keywordAuthorMAPKs-
dc.subject.keywordAuthornitric oxide-
dc.subject.keywordAuthorcyclooxygenase-2-
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