Artículo
Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration
Romero, Juan Ignacio
; Holubiec, Mariana Ines
; Logica Tornatore, Tamara Maite Ayelén
; Rivière, Stéphanie; Hanschmann, Eva Maria; Kolliker Frers, Rodolfo Alberto
; Tau, Julia
; Blanco, Eduardo; Galeano, Pablo
; Rodríguez de Fonseca, Fernando; Lillig, Christopher Horst; Capani, Francisco
Fecha de publicación:
06/2017
Editorial:
Hindawi Publishing Corporation
Revista:
Oxidative Medicine and Cellular Longevity
ISSN:
1942-0900
e-ISSN:
1942-0994
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury
Palabras clave:
Perinatal Asphyxia
,
Grx2
,
Treatment
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Articulos(IIBBA)
Articulos de INST.DE INVEST.BIOQUIMICAS DE BS.AS(I)
Articulos de INST.DE INVEST.BIOQUIMICAS DE BS.AS(I)
Citación
Romero, Juan Ignacio; Holubiec, Mariana Ines; Logica Tornatore, Tamara Maite Ayelén; Rivière, Stéphanie; Hanschmann, Eva Maria; et al.; Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration; Hindawi Publishing Corporation; Oxidative Medicine and Cellular Longevity; 2017; 6-2017; 1-14
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