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  4. Τμήμα Ιατρικής
  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/20274
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dc.contributor.authorXagorari, A.en
dc.contributor.authorPapapetropoulos, A.en
dc.contributor.authorMauromatis, A.en
dc.contributor.authorEconomou, M.en
dc.contributor.authorFotsis, T.en
dc.contributor.authorRoussos, C.en
dc.date.accessioned2015-11-24T19:05:57Z-
dc.date.available2015-11-24T19:05:57Z-
dc.identifier.issn0022-3565-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20274-
dc.rightsDefault Licence-
dc.subjectAnimalsen
dc.subjectBlotting, Westernen
dc.subjectCell Lineen
dc.subjectCytokines/*biosynthesisen
dc.subjectEndotoxins/*antagonists & inhibitors/toxicityen
dc.subjectFlavonoids/*pharmacologyen
dc.subjectInflammation/*metabolismen
dc.subjectInterleukin-6/metabolismen
dc.subjectLipopolysaccharides/*antagonists & inhibitors/toxicityen
dc.subjectLuteolinen
dc.subjectMacrophages/*drug effects/metabolismen
dc.subjectNF-kappa B/metabolismen
dc.subjectNitrites/metabolismen
dc.subjectOncogene Protein v-akten
dc.subjectPhosphorylationen
dc.subjectQuercetin/pharmacologyen
dc.subjectRatsen
dc.subjectRetroviridae Proteins, Oncogenic/metabolismen
dc.subjectTransfectionen
dc.subjectTumor Necrosis Factor-alpha/metabolismen
dc.subjectTyrosine/metabolismen
dc.titleLuteolin inhibits an endotoxin-stimulated phosphorylation cascade and proinflammatory cytokine production in macrophagesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11123379-
heal.identifier.secondaryhttp://jpet.aspetjournals.org/content/296/1/181.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2001-
heal.abstractFlavonoids are naturally occurring polyphenolic compounds with a wide distribution throughout the plant kingdom. In the present study, we compared the ability of several flavonoids to modulate the production of proinflammatory molecules from lipopolysaccharide (LPS)-stimulated macrophages and investigated their mechanism(s) of action. Pretreatment of RAW 264.7 with luteolin, luteolin-7-glucoside, quercetin, and the isoflavonoid genistein inhibited both the LPS-stimulated TNF-alpha and interleukin-6 release, whereas eriodictyol and hesperetin only inhibited TNF-alpha release. From the compounds tested luteolin and quercetin were the most potent in inhibiting cytokine production with an IC(50) of less than 1 and 5 microM for TNF-alpha release, respectively. To determine the mechanisms by which flavonoids inhibit LPS signaling, we used luteolin and determined its ability to interfere with total protein tyrosine phosphorylation as well as Akt phosphorylation and nuclear factor-kappaB activation. Pretreatment of the cells with luteolin attenuated LPS-induced tyrosine phosphorylation of many discrete proteins. Moreover, luteolin inhibited LPS-induced phosphorylation of Akt. Treatment of macrophages with LPS resulted in increased IkappaB-alpha phosphorylation and reduced the levels of IkappaB-alpha. Pretreatment of cells with luteolin abolished the effects of LPS on IkappaB-alpha. To determine the functional relevance of the phosphorylation events observed with IkappaB-alpha, macrophages were transfected either with a control vector or a vector coding for the luciferase reporter gene under the control of kappaB cis-acting elements. Incubation of transfected RAW 264.7 cells with LPS increased luciferase activity in a luteolin-sensitive manner. We conclude that luteolin inhibits protein tyrosine phosphorylation, nuclear factor-kappaB-mediated gene expression and proinflammatory cytokine production in murine macrophages.en
heal.journalNameJ Pharmacol Exp Theren
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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