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dc.contributor.authorNiloufar Ansari
dc.contributor.authorNiloufar Ansari
dc.contributor.authorFariba Khodagholi
dc.contributor.authorMohsen Amini
dc.date.accessioned2017-09-18T10:11:25Z
dc.date.available2017-09-18T10:11:25Z
dc.date.issued2011-05-11
dc.identifier.urihttp://dsp.sbmu.ac.ir/xmlui/handle/123456789/62794
dc.description.abstractApoptosis or programmed cell death has been suggested as an important mode of neurodegeneration in Alzheimer's disease pathogenesis. The present study explored the neuroprotective effect of 2-ethoxy-4,5-diphenyl-1,3-oxazine-6-one (EDPOO) against H 2 O 2 -induced cell death in rat pheochromocytoma (PC12) cells. We found that H 2 O 2 triggered a range of cellular cascades which leads to cell death, whereas pretreatment of the cells with this oxazine derivative attenuated the extent of apoptosis, as assessed by MTT assay, acridine orange/ethidium bromide staining and caspase-3 expression assay. We further showed that EDPOO exerts its neuroprotective effect by enhancing Hsp-70 level, stabilizing Nrf2 and upregulation of HO-1 and γ-GCS. Moreover, this oxazine derivative regulated cellular redox status via antioxidant enzyme upregulation. The neuroprotective effect of this compound may provide a new potential application for the treatment of neurodegenerative diseases. © 2011 Elsevier B.V. All rights reserved.
dc.sourceEuropean Journal of Pharmacology
dc.subjectAlzheimer's disease
dc.subjectApoptosis
dc.subjectNrf2
dc.subjectOxazine derivative
dc.subjectOxidative stress
dc.subjectPC12 cells
dc.title2-Ethoxy-4,5-diphenyl-1,3-oxazine-6-one activates the Nrf2/HO-1 axis and protects against oxidative stress-induced neuronal death
dc.journal.volume658
dc.journal.issue2-3
dc.identifier.doi10.1016/j.ejphar.2011.02.028
dc.journal.pages84-90
dc.contributor.authorid35738577700
dc.contributor.authorid35738577700
dc.contributor.authorid8354508500
dc.contributor.authorid7005942571
dc.contributor.citation35738577700|60018934|Niloufar Ansari
dc.contributor.citation35738577700|60018934|Niloufar Ansari
dc.contributor.citation8354508500|60018934|Fariba Khodagholi
dc.contributor.citation7005942571|60027708|Mohsen Amini
dc.contributor.affiliationid60018934
dc.contributor.affiliationid60018934
dc.contributor.affiliationid60018934
dc.contributor.affiliationid60027708


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