Ex vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Aß(1-42)

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dc.contributor.authorTurunc Bayrakdar E.
dc.contributor.authorArmagan G.
dc.contributor.authorUyanikgil Y.
dc.contributor.authorKanit L.
dc.contributor.authorKoylu E.
dc.contributor.authorYalcin A.
dc.date.accessioned2019-10-27T08:22:26Z
dc.date.available2019-10-27T08:22:26Z
dc.date.issued2014
dc.departmentEge Üniversitesien_US
dc.description.abstractAlzheimer's disease (AD) is the most common form of dementia and is characterized by the presence of senile plaques and neurofibrillary tangles, along with synaptic loss. The underlying mechanisms of AD are not clarified yet, but oxidative stress and mitochondrial dysfunction are important factors. Overactivation of poly(adenosine diphosphate ribose) polymerase-1 (PARP-1) enzyme has been known to cause neuroinflammation and cell death in neurodegenerative processes. The aim of the present study was to investigate the protective effects of the PARP-1 inhibitors, 3-aminobenzamide (3-AB) and nicotinamide (NA), against amyloid ß peptide (1-42) (Aß(1-42))-induced oxidative damage and mitochondrial reduction capacity on isolated synaptosomes. Rats were injected intraperitoneally with 3-AB (30-100mgkg-1), NA (100-500mgkg-1) or with saline for 7days. Synaptosomes were incubated with 10-30µM Aß(1-42) or saline for 6h at 37°C. Ex vivo Aß(1-42) treatment significantly induced oxidative stress and mitochondrial dysfunction in synaptosomes of the saline group, while synaptosomes of 3-AB and NA groups showed significant decreases in lipid peroxidation, reactive oxygen species production and protein oxidation. Moreover, both NA and 3-AB were able to improve the mitochondrial reduction capacity against Aß(1-42). These data suggest that NA and 3-AB may have protective effects in neurodegenerative processes because of the reduced levels of oxidative stress and the improvement of mitochondrial function. © 2014 John Wiley & Sons, Ltd..en_US
dc.identifier.doi10.1002/cbf.3049en_US
dc.identifier.endpage564en_US
dc.identifier.issn0263-6484
dc.identifier.issue7en_US
dc.identifier.pmid25111857en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage557en_US
dc.identifier.urihttps://doi.org/10.1002/cbf.3049
dc.identifier.urihttps://hdl.handle.net/11454/26249
dc.identifier.volume32en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherJohn Wiley and Sons Ltden_US
dc.relation.ispartofCell Biochemistry and Functionen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subject3-aminobenzamideen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectAmyloid ß peptide (1-42)en_US
dc.subjectNicotinamideen_US
dc.subjectOxidative stressen_US
dc.subjectPARP-1 inhibitionen_US
dc.subjectSynaptosomeen_US
dc.titleEx vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Aß(1-42)en_US
dc.typeArticleen_US

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