Por favor, use este identificador para citar o enlazar a este item:
http://hdl.handle.net/10261/343607
COMPARTIR / EXPORTAR:
SHARE CORE BASE | |
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE | |
Título: | Neuroprotection by glutamate oxaloacetate transaminase in ischemic stroke: An experimental study |
Autor: | Campos, Francisco CSIC; Sobrino, Tomás; Ramos-Cabrer, Pedro; Argibay, Bárbara; Agulla, Jesús CSIC ORCID; Pérez-Mato, María; Rodríguez-González, Raquel; Brea, David CSIC ORCID ; Castillo, José | Palabras clave: | Animal model of ischemia Glutamate Glutamate oxaloacetate transaminase Magnetic resonance Neuroprotection |
Fecha de publicación: | jun-2011 | Editor: | Sage Publications | Citación: | Journal of Cerebral Blood Flow and Metabolism 31(6): 1378-1386 (2011) | Resumen: | As ischemic stroke is associated with an excessive release of glutamate into the neuronal extracellular space, a decrease in blood glutamate levels could provide a mechanism to remove it from the brain tissue, by increasing the brain-blood gradient. In this regard, the ability of glutamate oxaloacetate transaminase (GOT) to metabolize glutamate in blood could represent a potential neuroprotective tool for ischemic stroke. This study aimed to determine the neuroprotective effects of GOT in an animal model of cerebral ischemia by means of a middle cerebral arterial occlusion (MCAO) following the Stroke Therapy Academic Industry Roundtable (STAIR) group guidelines. In this animal model, oxaloacetate-mediated GOT activation inhibited the increase of blood and cerebral glutamate after MCAO. This effect is reflected in a reduction of infarct size, smaller edema volume, and lower sensorimotor deficits with respect to controls. Magnetic resonance spectroscopy confirmed that the increase of glutamate levels in the brain parenchyma after MCAO is inhibited after oxaloacetate-mediated GOT activation. These findings show the capacity of the GOT to remove glutamate from the brain by means of blood glutamate degradation, and suggest the applicability of this enzyme as an efficient and novel neuroprotective tool against ischemic stroke. | Versión del editor: | https://doi.org/10.1038/jcbfm.2011.3 | URI: | http://hdl.handle.net/10261/343607 | DOI: | 10.1038/jcbfm.2011.3 | ISSN: | 0271-678X | E-ISSN: | 1559-7016 |
Aparece en las colecciones: | (IIBB) Artículos |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
---|---|---|---|---|
Campos et al 2011.pdf | 737,21 kB | Adobe PDF | Visualizar/Abrir |
CORE Recommender
PubMed Central
Citations
55
checked on 11-abr-2024
SCOPUSTM
Citations
115
checked on 25-abr-2024
WEB OF SCIENCETM
Citations
106
checked on 25-feb-2024
Page view(s)
18
checked on 26-abr-2024
Download(s)
3
checked on 26-abr-2024
Google ScholarTM
Check
Altmetric
Altmetric
Artículos relacionados:
NOTA: Los ítems de Digital.CSIC están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.