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Citation
Tags
HERO ID
2970939
Reference Type
Journal Article
Title
Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice
Author(s)
Yang, J; Ahn, HN; Chang, M; Narasimhan, P; Chan, PH; Song, YS
Year
2013
Is Peer Reviewed?
Yes
Journal
Journal of Neurochemistry
ISSN:
0022-3042
EISSN:
1471-4159
Volume
124
Issue
4
Page Numbers
523-535
Language
English
PMID
23199288
DOI
10.1111/jnc.12111
Web of Science Id
WOS:000314186300010
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.
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