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dc.contributor.authorGodoy J.A.
dc.contributor.authorLindsay C.B.
dc.contributor.authorQuintanilla R.A.
dc.contributor.authorCarvajal F.J.
dc.contributor.authorCerpa W.
dc.contributor.authorInestrosa N.C.
dc.date.accessioned2020-09-02T22:19:17Z
dc.date.available2020-09-02T22:19:17Z
dc.date.issued2017
dc.identifier10.1007/s12035-016-0203-x
dc.identifier.citation54, 9, 7116-7128
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4686
dc.descriptionAmyloid-β peptide (Aβ) is one of the major players in the pathogenesis of Alzheimer’s disease (AD). Despite numerous studies, the mechanisms by which Aβ induces neurodegeneration are not completely understood. Oxidative stress is considered a major contributor to the pathogenesis of AD, and accumulating evidence indicates that high levels of reactive oxygen species (ROS) are involved in Aβ-induced neurodegeneration. Moreover, Aβ can induce the deregulation of calcium homeostasis, which also affects mitochondrial function and triggers neuronal cell death. In the present study, we analyzed the effects of quercetin, a plant flavonoid with antioxidant properties, on oxidative stress- and Aβ-induced degeneration. Our results indicate that quercetin efficiently protected against H2O2-induced neuronal toxicity; however, this protection was only partial in rat hippocampal neurons that were treated with Aβ. Treatment with quercetin decreased ROS levels, recovered the normal morphology of mitochondria, and prevented mitochondrial dysfunction in neurons that were treated with H2O2. By contrast, quercetin treatment partially rescued hippocampal neurons from Aβ-induced mitochondrial injury. Most importantly, quercetin treatment prevented the toxic effects that are induced by H2O2 in hippocampal neurons and, to a lesser extent, the Aβ-induced toxicity that is associated with the superoxide anion, which is a precursor of ROS production in mitochondria. Collectively, these results indicate that quercetin exerts differential effects on the prevention of H2O2- and Aβ-induced neurotoxicity in hippocampal neurons and may be a powerful tool for dissecting the molecular mechanisms underlying Aβ neurotoxicity. © 2016, Springer Science+Business Media New York.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectAlzheimer’s disease
dc.subjectOxidative stress
dc.subjectQuercetin
dc.subjectSod−/+ mice
dc.subjectΑβ aggregates
dc.subjectamyloid beta protein
dc.subjecthydrogen peroxide
dc.subjectquercetin
dc.subjectagents interacting with transmitter, hormone or drug receptors
dc.subjectamyloid beta protein
dc.subjecthydrogen peroxide
dc.subjectneuroprotective agent
dc.subjectprotein aggregate
dc.subjectquercetin
dc.subjectreactive oxygen metabolite
dc.subjectsuperoxide dismutase
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbrain mitochondrion
dc.subjectbrain nerve cell
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectdrug determination
dc.subjectdrug effect
dc.subjectembryo
dc.subjecthippocampal neuron
dc.subjectmitochondrial membrane potential
dc.subjectmolecular dynamics
dc.subjectneuroprotection
dc.subjectneurotoxicity
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectprotein aggregation
dc.subjectrat
dc.subjectanimal
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectnerve cell
dc.subjectnerve ending
dc.subjectneuroprotection
dc.subjectpathology
dc.subjectSprague Dawley rat
dc.subjecttransgenic mouse
dc.subjectAmyloid beta-Peptides
dc.subjectAnimals
dc.subjectHippocampus
dc.subjectHydrogen Peroxide
dc.subjectMembrane Potential, Mitochondrial
dc.subjectMice, Transgenic
dc.subjectMitochondria
dc.subjectNeurons
dc.subjectNeuroprotection
dc.subjectNeuroprotective Agents
dc.subjectNeurotransmitter Agents
dc.subjectOxidative Stress
dc.subjectPresynaptic Terminals
dc.subjectProtein Aggregates
dc.subjectQuercetin
dc.subjectRats, Sprague-Dawley
dc.subjectReactive Oxygen Species
dc.subjectSuperoxide Dismutase
dc.titleQuercetin Exerts Differential Neuroprotective Effects Against H2O2 and Aβ Aggregates in Hippocampal Neurons: the Role of Mitochondria
dc.typeArticle


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