Effects of apigenin, lycopene and astaxanthin on 7β-hydroxycholesterol-induced apoptosis and Akt phosphorylation in U937 cells

dc.contributor.authorLordan, Sinéad
dc.contributor.authorO'Neill, Cora
dc.contributor.authorO'Brien, Nora M.
dc.contributor.funderHigher Education Authorityen
dc.date.accessioned2009-09-17T13:50:15Z
dc.date.available2009-09-17T13:50:15Z
dc.date.copyright2008
dc.date.issued2008-08
dc.description.abstractOxysterols arise from the enzymic or non-enzymic oxidation of cholesterol and have been shown to be cytotoxic to certain cell lines. In particular, apoptosis induced by the oxysterol 7β-hydroxycholesterol (7β-OH) has been associated with the generation of oxidative stress, cytochrome c release and caspase activation. Due to the fundamental importance of apoptosis in pathological processes, the identification of substances capable of modulating this form of cell death is now actively researched. The objective of the present study was to investigate if apigenin, lycopene and astaxanthin could inhibit 7β-OH-induced apoptosis in U937 cells. Pretreatment with 0.1 µM-astaxanthin protected against apoptosis, while lycopene did not oppose the adverse effects of 7β-OH. At low concentrations, apigenin did not protect against oxysterol-induced apoptosis; however, at higher concentrations it intensified cell death. Additionally, we investigated the effect of 7β-OH, apigenin and astaxanthin on the activation of the serine threonine kinase Akt (phosphorylated Akt:Akt ratio) to determine whether the effect on cell viability and growth was linked to the Akt signalling pathway. Akt activation was decreased in the oxysterol-treated cells compared with control cells; however, this did not attain significance. Interestingly, activation of Akt was significantly reduced compared with control cells following incubation with apigenin and astaxanthin both in the absence and in the presence of 7β-OH. Our data suggest that apigenin, lycopene and astaxanthin failed to protect against 7β-OH-induced apoptosis, and the decrease in cell viability and the increase in apoptotic nuclei induced by the antioxidants appear to be associated with down regulation of Akt activity.en
dc.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationLordan, S., O’ Neill, C. and O’ Brien, N.M. (2008) Effects of apigenin, lycopene and astaxanthin on 7-beta-hydroxycholesterol-induced apoptosis and Akt phosphorylation in U937 cells. British Journal of Nutrition, 100: 287-296en
dc.identifier.doi10.1017/S0007114507898643
dc.identifier.endpage296en
dc.identifier.issn0007-1145
dc.identifier.issued2en
dc.identifier.journaltitleBritish Journal of Nutritionen
dc.identifier.startpage287en
dc.identifier.urihttps://hdl.handle.net/10468/69
dc.identifier.volume100en
dc.language.isoenen
dc.publisherCambridge University Pressen
dc.rights© The Authors 2008en
dc.subjectAkten
dc.subjectCytotoxicityen
dc.subject7β-Hydroxycholesterolen
dc.subject.lcshAntioxidantsen
dc.subject.lcshProtein kinasesen
dc.subject.lcshApoptosisen
dc.subject.lcshOxysterolsen
dc.titleEffects of apigenin, lycopene and astaxanthin on 7β-hydroxycholesterol-induced apoptosis and Akt phosphorylation in U937 cellsen
dc.typeArticle (peer-reviewed)en
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