Luteolin reduces lipopolysaccharide-induced lethal toxicity and expression of proinflammatory molecules in mice

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dc.contributor.authorKotanidou, A.en
dc.contributor.authorXagorari, A.en
dc.contributor.authorBagli, E.en
dc.contributor.authorKitsanta, P.en
dc.contributor.authorFotsis, T.en
dc.contributor.authorPapapetropoulos, A.en
dc.contributor.authorRoussos, C.en
dc.date.accessioned2015-11-24T19:05:56Z
dc.date.available2015-11-24T19:05:56Z
dc.identifier.issn1073-449X-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/20272
dc.rightsDefault Licence-
dc.subjectAnalysis of Varianceen
dc.subjectAnimalsen
dc.subjectFemaleen
dc.subjectFlavonoids/*pharmacologyen
dc.subjectIntercellular Adhesion Molecule-1/blood/*drug effectsen
dc.subjectInterleukin-6/blooden
dc.subjectLeukocytes/drug effects/metabolismen
dc.subjectLipopolysaccharides/*immunologyen
dc.subjectLiver/pathologyen
dc.subjectLung/pathologyen
dc.subjectLuteolinen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectSepsis/*drug therapy/immunology/mortalityen
dc.subjectSurvival Analysisen
dc.subjectTumor Necrosis Factor-alpha/*drug effects/metabolismen
dc.titleLuteolin reduces lipopolysaccharide-induced lethal toxicity and expression of proinflammatory molecules in miceen
heal.abstractLuteolin is a flavonoid that has been shown to reduce proinflammatory molecule expression in vitro. In the present study, we have tested the ability of luteolin to inhibit lipopolysaccharide (LPS)- induced lethal toxicity and proinflammatory molecule expression in vivo. Mice receiving LPS (Salmonella enteriditis LPS, 32 mg/kg, intraperitoneally) exhibited high mortality with only 4.1% of the animals surviving seven days after the LPS challenge. On the contrary, mice that had received luteolin (0.2 mg/kg, intraperitoneally) before LPS showed an increased survival rate with 48% remaining alive on Day 7. To investigate the mechanism by which luteolin affords protection against LPS toxicity we measured intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF-alpha) production in response to LPS in the presence or absence of luteolin pretreatment. Treatment of animals with LPS increased serum TNF-alpha levels in a time-dependent manner. The increase in peak serum TNF-alpha levels was sensitive to luteolin pretreatment. Luteolin pretreatment also reduced LPS-stimulated ICAM-1 expression in the liver and abolished leukocyte infiltration in the liver and lung. We conclude that luteolin protects against LPS-induced lethal toxicity, possibly by inhibiting proinflammatory molecule (TNF-alpha, ICAM-1) expression in vivo and reducing leukocyte infiltration in tissues.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11897650-
heal.identifier.secondaryhttp://ajrccm.atsjournals.org/content/165/6/818.full.pdf-
heal.journalNameAm J Respir Crit Care Meden
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2002-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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