Anti-apoptotic and anti-oxidative roles of quercetin after traumatic brain injury.
Cell Mol Neurobiol
; 34(6): 797-804, 2014 Aug.
Article
em En
| MEDLINE
| ID: mdl-24846663
ABSTRACT
Experimental studies have demonstrated significant secondary damage (including cell apoptosis, blood-brain barrier disruption, inflammatory responses, excitotoxic damage, and free radical production) after traumatic brain injury (TBI). Quercetin is a natural flavonoid found in high quantities in fruits and vegetables, and may be a potential antioxidant and free radical scavenger. The purpose of this study was to determine the effects of quercetin on TBI-induced upregulation of oxidative stress, inflammation, and apoptosis in adult Sprague-Dawley rats. Animals were subjected to Feeney's weight-drop injury, thus inducing the parietal contusion brain injury model. Quercetin was administered (30 mg/kg intraperitoneal injection) 0, 24, 48, and 72 h after TBI. Quercetin reduced cognitive deficits, the number of TUNEL- and ED-1-positive cells, the protein expressions of Bax and cleaved-caspase-3 proteins, and the levels of TBARS and proinflammatory cytokines, and increased the activity of antioxidant enzymes (GSH-Px, SOD, and CAT) at 1 week after TBI. Our results suggest that in TBI rats, quercetin improves cognitive function owing to its neuroprotective action via the inhibition of oxidative stress, leading to a reduced inflammatory response, thereby reducing neuronal death.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Quercetina
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Lesões Encefálicas
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Apoptose
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Estresse Oxidativo
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Antioxidantes
Limite:
Animals
Idioma:
En
Revista:
Cell Mol Neurobiol
Ano de publicação:
2014
Tipo de documento:
Article
País de afiliação:
China