Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice
DC Field | Value | Language |
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dc.contributor.author | Yang, Jiwon | - |
dc.contributor.author | Ahn, Hye-na | - |
dc.contributor.author | Chang, Minsun | - |
dc.contributor.author | Narasimhan, Purnima | - |
dc.contributor.author | Chan, Pak H. | - |
dc.contributor.author | Song, Yun Seon | - |
dc.date.available | 2021-02-22T12:17:01Z | - |
dc.date.issued | 2013-02 | - |
dc.identifier.issn | 0022-3042 | - |
dc.identifier.issn | 1471-4159 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11363 | - |
dc.description.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. | - |
dc.format.extent | 13 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.title | Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/jnc.12111 | - |
dc.identifier.scopusid | 2-s2.0-84873302973 | - |
dc.identifier.wosid | 000314186300010 | - |
dc.identifier.bibliographicCitation | JOURNAL OF NEUROCHEMISTRY, v.124, no.4, pp 523 - 535 | - |
dc.citation.title | JOURNAL OF NEUROCHEMISTRY | - |
dc.citation.volume | 124 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 523 | - |
dc.citation.endPage | 535 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.subject.keywordPlus | SUPEROXIDE DISMUTASE ACTIVITY | - |
dc.subject.keywordPlus | FIBRILLARY ACIDIC PROTEIN | - |
dc.subject.keywordPlus | TRAUMATIC BRAIN-INJURY | - |
dc.subject.keywordPlus | N-TERT-BUTYLNITRONE | - |
dc.subject.keywordPlus | EXPERIMENTAL STROKE | - |
dc.subject.keywordPlus | ALTERNATIVE PATHWAY | - |
dc.subject.keywordPlus | LIVER-REGENERATION | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordAuthor | antioxidant | - |
dc.subject.keywordAuthor | complement component 3 | - |
dc.subject.keywordAuthor | focal cerebral ischemia | - |
dc.subject.keywordAuthor | oxidative stress | - |
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