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Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice.
Yang, Jiwon; Ahn, Hye-Na; Chang, Minsun; Narasimhan, Purnima; Chan, Pak H; Song, Yun Seon.
Afiliación
  • Yang J; Department of Pharmacology, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.
J Neurochem ; 124(4): 523-35, 2013 Feb.
Article en En | MEDLINE | ID: mdl-23199288
ABSTRACT
Oxidative stress after stroke is associated with the inflammatory system activation in the brain. The complement cascade, especially the degradation products of complement component 3, is a key inflammatory mediator of cerebral ischemia. We have shown that pro-inflammatory complement component 3 is increased by oxidative stress after ischemic stroke in mice using DNA array. In this study, we investigated whether up-regulation of complement component 3 is directly related to oxidative stress after transient focal cerebral ischemia in mice and oxygen-glucose deprivation in brain cells. Persistent up-regulation of complement component 3 expression was reduced in copper/zinc-superoxide dismutase transgenic mice, and manganese-superoxide dismutase knock-out mice showed highly increased complement component 3 levels after transient focal cerebral ischemia. Antioxidant N-tert-butyl-α-phenylnitrone treatment suppressed complement component 3 expression after transient focal cerebral ischemia. Accumulation of complement component 3 in neurons and microglia was decreased by N-tert-butyl-α-phenylnitrone, which reduced infarct volume and impaired neurological deficiency after cerebral ischemia and reperfusion in mice. Small interfering RNA specific for complement component 3 transfection showed a significant increase in brain cells viability after oxygen-glucose deprivation. Our study suggests that the neuroprotective effect of antioxidants through complement component 3 suppression is a new strategy for potential therapeutic approaches in stroke.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Complemento C3 / Daño por Reperfusión / Regulación hacia Arriba / Isquemia Encefálica / Fármacos Neuroprotectores / Óxidos N-Cíclicos / Neuronas Tipo de estudio: Etiology_studies / Prognostic_studies Idioma: En Revista: J Neurochem Año: 2013 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Complemento C3 / Daño por Reperfusión / Regulación hacia Arriba / Isquemia Encefálica / Fármacos Neuroprotectores / Óxidos N-Cíclicos / Neuronas Tipo de estudio: Etiology_studies / Prognostic_studies Idioma: En Revista: J Neurochem Año: 2013 Tipo del documento: Article