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The complement cascade, especially the degradation products of complement component 3, is a key inflammatory mediator of cerebral ischemia. We have shown that pro\u2010inflammatory complement component 3 is increased by oxidative stress after ischemic stroke in mice using <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> array. In this study, we investigated whether up\u2010regulation of complement component 3 is directly related to oxidative stress after transient focal cerebral ischemia in mice and oxygen\u2010glucose deprivation in brain cells. Persistent up\u2010regulation of complement component 3 expression was reduced in copper\/zinc\u2010superoxide dismutase transgenic mice, and manganese\u2010superoxide dismutase knock\u2010out mice showed highly increased complement component 3 levels after transient focal cerebral ischemia. Antioxidant <jats:italic>N\u2010tert<\/jats:italic>\u2010butyl\u2010\u03b1\u2010phenylnitrone treatment suppressed complement component 3 expression after transient focal cerebral ischemia. Accumulation of complement component 3 in neurons and microglia was decreased by <jats:italic>N\u2010tert<\/jats:italic>\u2010butyl\u2010\u03b1\u2010phenylnitrone, which reduced infarct volume and impaired neurological deficiency after cerebral ischemia and reperfusion in mice. Small interfering <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> specific for complement component 3 transfection showed a significant increase in brain cells viability after oxygen\u2010glucose 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.<\/jats:p>","DOI":"10.1111\/jnc.12111","type":"journal-article","created":{"date-parts":[[2012,12,1]],"date-time":"2012-12-01T08:49:08Z","timestamp":1354351748000},"page":"523-535","source":"Crossref","is-referenced-by-count":53,"title":["Complement component 3 inhibition by an antioxidant is neuroprotective after cerebral ischemia and reperfusion in mice"],"prefix":"10.1111","volume":"124","author":[{"given":"Jiwon","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Pharmacology College of Pharmacy Sookmyung Women's University Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye\u2010na","family":"Ahn","sequence":"additional","affiliation":[{"name":"Department of Pharmacology College of Pharmacy Sookmyung Women's University Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minsun","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Medical and Pharmaceutical Science College of Science Sookmyung Women's University Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Purnima","family":"Narasimhan","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Department of Neurology and Neurological Sciences, and Program in Neurosciences Stanford University School of Medicine Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pak H.","family":"Chan","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Department of Neurology and Neurological Sciences, and Program in Neurosciences Stanford University School of Medicine Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun Seon","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Pharmacology College of Pharmacy Sookmyung Women's University Seoul Republic of Korea"},{"name":"Department of Neurosurgery Department of Neurology and Neurological Sciences, and Program in Neurosciences Stanford University School of Medicine Stanford California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,12,28]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1747-4949.2009.00387.x"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0045801"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0700506104"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2008.07.015"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.2003.tb03138.x"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1098-1136(20000101)29:1<91::AID-GLIA9>3.0.CO;2-I"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0008433"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0898-6568(00)00111-X"},{"key":"e_1_2_7_10_1","first-page":"77","article-title":"Changes in plasma levels of complement in patients with acute ischemic stroke","volume":"46","author":"Cojocaru I. 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