Mostrar el registro sencillo del ítem
Quercetin Exerts Differential Neuroprotective Effects Against H2O2 and Aβ Aggregates in Hippocampal Neurons: the Role of Mitochondria
dc.contributor.author | Godoy J.A. | |
dc.contributor.author | Lindsay C.B. | |
dc.contributor.author | Quintanilla R.A. | |
dc.contributor.author | Carvajal F.J. | |
dc.contributor.author | Cerpa W. | |
dc.contributor.author | Inestrosa N.C. | |
dc.date.accessioned | 2020-09-02T22:19:17Z | |
dc.date.available | 2020-09-02T22:19:17Z | |
dc.date.issued | 2017 | |
dc.identifier | 10.1007/s12035-016-0203-x | |
dc.identifier.citation | 54, 9, 7116-7128 | |
dc.identifier.issn | 08937648 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4686 | |
dc.description | Amyloid-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.iso | en | |
dc.publisher | Humana Press Inc. | |
dc.subject | Alzheimer’s disease | |
dc.subject | Oxidative stress | |
dc.subject | Quercetin | |
dc.subject | Sod−/+ mice | |
dc.subject | Αβ aggregates | |
dc.subject | amyloid beta protein | |
dc.subject | hydrogen peroxide | |
dc.subject | quercetin | |
dc.subject | agents interacting with transmitter, hormone or drug receptors | |
dc.subject | amyloid beta protein | |
dc.subject | hydrogen peroxide | |
dc.subject | neuroprotective agent | |
dc.subject | protein aggregate | |
dc.subject | quercetin | |
dc.subject | reactive oxygen metabolite | |
dc.subject | superoxide dismutase | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal tissue | |
dc.subject | Article | |
dc.subject | brain mitochondrion | |
dc.subject | brain nerve cell | |
dc.subject | cell viability | |
dc.subject | controlled study | |
dc.subject | drug determination | |
dc.subject | drug effect | |
dc.subject | embryo | |
dc.subject | hippocampal neuron | |
dc.subject | mitochondrial membrane potential | |
dc.subject | molecular dynamics | |
dc.subject | neuroprotection | |
dc.subject | neurotoxicity | |
dc.subject | nonhuman | |
dc.subject | oxidative stress | |
dc.subject | protein aggregation | |
dc.subject | rat | |
dc.subject | animal | |
dc.subject | hippocampus | |
dc.subject | metabolism | |
dc.subject | mitochondrion | |
dc.subject | nerve cell | |
dc.subject | nerve ending | |
dc.subject | neuroprotection | |
dc.subject | pathology | |
dc.subject | Sprague Dawley rat | |
dc.subject | transgenic mouse | |
dc.subject | Amyloid beta-Peptides | |
dc.subject | Animals | |
dc.subject | Hippocampus | |
dc.subject | Hydrogen Peroxide | |
dc.subject | Membrane Potential, Mitochondrial | |
dc.subject | Mice, Transgenic | |
dc.subject | Mitochondria | |
dc.subject | Neurons | |
dc.subject | Neuroprotection | |
dc.subject | Neuroprotective Agents | |
dc.subject | Neurotransmitter Agents | |
dc.subject | Oxidative Stress | |
dc.subject | Presynaptic Terminals | |
dc.subject | Protein Aggregates | |
dc.subject | Quercetin | |
dc.subject | Rats, Sprague-Dawley | |
dc.subject | Reactive Oxygen Species | |
dc.subject | Superoxide Dismutase | |
dc.title | Quercetin Exerts Differential Neuroprotective Effects Against H2O2 and Aβ Aggregates in Hippocampal Neurons: the Role of Mitochondria | |
dc.type | Article |