Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18492
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dc.contributor.authorKolettas, E.en
dc.contributor.authorThomas, C.en
dc.contributor.authorLeneti, E.en
dc.contributor.authorSkoufos, I.en
dc.contributor.authorMbatsi, C.en
dc.contributor.authorSisoula, C.en
dc.contributor.authorManos, G.en
dc.contributor.authorEvangelou, A.en
dc.date.accessioned2015-11-24T18:53:05Z-
dc.date.available2015-11-24T18:53:05Z-
dc.identifier.issn0300-8177-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18492-
dc.rightsDefault Licence-
dc.subjectAntioxidants/pharmacologyen
dc.subjectApoptosis/*drug effectsen
dc.subjectApoptosis Regulatory Proteins/metabolismen
dc.subjectCell Proliferation/drug effectsen
dc.subjectCinnamates/*pharmacologyen
dc.subjectDepsidesen
dc.subjectDose-Response Relationship, Drugen
dc.subjectHumansen
dc.subjectHydrogen Peroxide/*pharmacologyen
dc.subjectJurkat Cells/*drug effectsen
dc.subjectProto-Oncogene Proteins c-bcl-2/*physiologyen
dc.titleRosmarinic acid failed to suppress hydrogen peroxide-mediated apoptosis but induced apoptosis of Jurkat cells which was suppressed by Bcl-2en
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1007/s11010-005-9064-8-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/16534555-
heal.identifier.secondaryhttp://www.springerlink.com/content/996237173447l435/fulltext.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2006-
heal.abstractRosmarinic acid (RosA), frequently found as a secondary metabolite in herbs and medicinal plants, has exhibited antioxidative and anti-inflammatory activities. RosA was shown to inhibit the proliferation and induce apoptosis of Jurkat T cells but the mechanism of action of RosA in apoptosis remains elusive. RosA inhibited the proliferation of Jurkat cells in a dose-dependent manner by suppressing the expression of cyclin D3 and p21(Cip1/Waf1) and up-regulating p27(Kip1). RosA induced apoptosis of Jurkat cells in a dose-dependent manner and failed to protect them from hydrogen peroxide (H2O2)-mediated apoptosis. Induction of apoptosis by RosA correlated with suppression of Bcl-2 but not of Bak or PUMA. Overexpression of Bcl-2 protected Jurkat cells from both H2O2- and RosA-induced apoptosis by altering the ratio of anti- to pro-apoptotic members of the Bcl-2 family. In conclusion, RosA inhibited Jurkat cell proliferation by altering the expression of cyclins and cyclin-dependent kinase inhibitors and induced apoptosis most likely acting through the mitochondrial pathway and possessed no anti-oxidant properties.en
heal.journalNameMol Cell Biochemen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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