Hematein inhibits atherosclerosis by inhibition of reactive oxygen generation and NF-κB-dependent inflammatory mediators in hyperlipidemic mice

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dc.contributor.authorJ H Choi-
dc.contributor.authorTae Sook Jeong-
dc.contributor.authorD Y Kim-
dc.contributor.authorY M Kim-
dc.contributor.authorH J Na-
dc.contributor.authorKi Hoan Nam-
dc.contributor.authorSae Bom Lee-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorSei Ryang Oh-
dc.contributor.authorYang Kyu Choi-
dc.contributor.authorSong Hae Bok-
dc.contributor.authorGoo Taeg Oh-
dc.date.accessioned2017-04-19T09:00:09Z-
dc.date.available2017-04-19T09:00:09Z-
dc.date.issued2003-
dc.identifier.issn0160-2446-
dc.identifier.uri10.1097/00005344-200308000-00019ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/6193-
dc.description.abstractHematein, a natural compound, is a known antiinflammatory and antiatherogenic agent in the rabbit model. The authors investigated the effects of this compound on atherogenesis and possible mechanisms of the actions in the hyperlipidemic mice. Low-density lipoprotein receptor-deficient (Ldlr-/-) mice fed a high-cholesterol diet alone for 8 weeks developed the fatty streak lesion in the aortic sinus, whereas this lesion was significantly reduced by hematein treatment without a change in plasma lipid levels compared with control mice. Hematein treatment reduced plasma levels of lipid peroxide and superoxide generation in LPS-stimulated peritoneal macrophage. Hematein treatment inhibited NF-κB-DNA binding activity in peritoneal macrophages from Ldlr-/- mice and the activation of NF-κB in RAW264.7 macrophages. This compound suppressed plasma nitrite/nitrate levels in Ldlr-/- mice and NO production and iNOS expression in LPS+IFNγ-stimulated peritoneal macrophages. Hematein treatment also suppressed the activity of iNOS promoters in RAW264.7 macrophages, and reduced the plasma levels of TNF-α and IL-1β and the production of these cytokines in LPS+IFNγ-stimulated peritoneal macrophages. These results suggest that hematein inhibits atherosclerotic lesion formation, possibly by reducing proinflammatory mediators through a decrease in reactive oxygen species generation and NF-κB activation.-
dc.publisherKluwer-
dc.titleHematein inhibits atherosclerosis by inhibition of reactive oxygen generation and NF-κB-dependent inflammatory mediators in hyperlipidemic mice-
dc.title.alternativeHematein inhibits atherosclerosis by inhibition of reactive oxygen generation and NF-κB-dependent inflammatory mediators in hyperlipidemic mice-
dc.typeArticle-
dc.citation.titleJournal of Cardiovascular Pharmacology-
dc.citation.number2-
dc.citation.endPage295-
dc.citation.startPage287-
dc.citation.volume42-
dc.contributor.affiliatedAuthorTae Sook Jeong-
dc.contributor.affiliatedAuthorKi Hoan Nam-
dc.contributor.affiliatedAuthorSae Bom Lee-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.affiliatedAuthorSei Ryang Oh-
dc.contributor.affiliatedAuthorYang Kyu Choi-
dc.contributor.affiliatedAuthorSong Hae Bok-
dc.contributor.affiliatedAuthorGoo Taeg Oh-
dc.contributor.alternativeName최재훈-
dc.contributor.alternativeName정태숙-
dc.contributor.alternativeName김대영-
dc.contributor.alternativeName김영명-
dc.contributor.alternativeName나희준-
dc.contributor.alternativeName남기환-
dc.contributor.alternativeName이새봄-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName최양규-
dc.contributor.alternativeName복성해-
dc.contributor.alternativeName오구택-
dc.identifier.bibliographicCitationJournal of Cardiovascular Pharmacology, vol. 42, no. 2, pp. 287-295-
dc.identifier.doi10.1097/00005344-200308000-00019-
dc.subject.keywordAnti-inflammation-
dc.subject.keywordAntiatherogenesis-
dc.subject.keywordHematein-
dc.subject.keywordNF-κB-
dc.subject.keywordReactive oxygen species-
dc.subject.localantiinflammation-
dc.subject.localAntiinflammation-
dc.subject.localanti-inflammation-
dc.subject.localAnti-Inflammation-
dc.subject.localAnti-inflammation-
dc.subject.localAntiatherogenesis-
dc.subject.localHematein-
dc.subject.localhematein-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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