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dc.creatorTovilović, Gordana
dc.creatorZogovic, Nevena
dc.creatorHarhaji-Trajković, Ljubica
dc.creatorMisirkić-Marjanović, Maja
dc.creatorJanjetovic, Kristina
dc.creatorVucicevic, Ljubica
dc.creatorKostić Rajačić, Slađana
dc.creatorSchrattenholz, Andre
dc.creatorIsaković, Aleksandra
dc.creatorŠoškić, Vukić
dc.creatorTrajković, Vladimir
dc.date.accessioned2019-01-30T17:31:06Z
dc.date.available2019-01-30T17:31:06Z
dc.date.issued2012
dc.identifier.issn1860-7179
dc.identifier.urihttps://cer.ihtm.bg.ac.rs/handle/123456789/1037
dc.description.abstractThe protective ability of novel arylpiperazine-based dopaminergic ligands against nitric oxide (NO)-mediated neurotoxicity is investigated. The most potent neuroprotective arylpiperazine identified during the study was N-{4-[2-(4-phenyl-piperazin-1-yl)ethyl]-phenyl}picolinamide, which protected SH-SY5Y human neuron-like cells from the proapoptotic effect of NO donor sodium nitroprusside (SNP) by decreasing oxidative stress, mitochondrial membrane depolarization, caspase activation and subsequent phosphatydilserine externalization/DNA fragmentation. The protective effect was associated with the inhibition of proapoptotic (JNK, ERK, AMPK) and activation of antiapoptotic (Akt) signaling pathways, in the absence of interference with intracellular NO accumulation. The neuroprotective action of arylpiperazines was shown to be independent of dopamine receptor binding, as it was not affected by the high-affinity D1/D2 receptor blocker butaclamol. These results reported support the further study of arylpiperazines as potential neuroprotective agents.en
dc.publisherWiley-V C H Verlag Gmbh, Weinheim
dc.relationinfo:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41025/RS//
dc.rightsrestrictedAccess
dc.sourceChemmedchem
dc.subjectapoptosisen
dc.subjectdopaminergic ligandsen
dc.subjectneuroprotectionen
dc.subjectnitric oxideen
dc.subjectnitrogen heterocyclesen
dc.titleArylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosisen
dc.typearticle
dc.rights.licenseARR
dcterms.abstractЈањетовиц, Кристина; Вуцицевиц, Љубица; Мисиркиц-Марјановиц, Маја; Хархаји-Трајковиц, Љубица; Зоговиц, Невена; Товиловиц, Гордана; Костић Рајачић, Слађана; Исаковиц, Aлександра; Трајковиц, Владимир; Сцхраттенхолз, Aндре; Соскиц, Вукиц;
dc.citation.volume7
dc.citation.issue3
dc.citation.spage495
dc.citation.epage508
dc.citation.other7(3): 495-508
dc.citation.rankM22
dc.identifier.pmid22298298
dc.identifier.doi10.1002/cmdc.201100537
dc.identifier.scopus2-s2.0-84857772680
dc.identifier.wos000300942300017
dc.type.versionpublishedVersion


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