Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice
- Authors
- Yang, Jiwon; Ahn, Hye-na; Chang, Minsun; Narasimhan, Purnima; Chan, Pak H.; Song, Yun Seon
- Issue Date
- Feb-2013
- Publisher
- WILEY-BLACKWELL
- Keywords
- antioxidant; complement component 3; focal cerebral ischemia; oxidative stress
- Citation
- JOURNAL OF NEUROCHEMISTRY, v.124, no.4, pp 523 - 535
- Pages
- 13
- Journal Title
- JOURNAL OF NEUROCHEMISTRY
- Volume
- 124
- Number
- 4
- Start Page
- 523
- End Page
- 535
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11363
- DOI
- 10.1111/jnc.12111
- ISSN
- 0022-3042
1471-4159
- 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-a-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-a-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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