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Antioxidant CR-6 protects against reperfusion injury after a transient episode of focal brain ischemia in rats

AuthorsPérez-Asensio, Fernando J. ; Rosa, Xavier de la ; Gorina, Roser ; Martínez, Emili ; Messeguer Peypoch, Ángel; Vila, Elisabet; Chamorro, Ángel; Planas, Anna M.
Issue DateMar-2010
PublisherNature Publishing Group
CitationJournal of Cerebral Blood Flow and Metabolism 30(3): 638-652 (2010)
AbstractOxidative and nitrosative stress are targets for intervention after ischemia/reperfusion. The aim of this study was to explore the effect of CR-6, a vitamin-E analogue that is antioxidant and scavenger of nitrogen-reactive species. Sprague–Dawley rats had the middle cerebral artery (MCA) occluded either for 90 mins or permanently. Cortical perfusion was continuously monitored by laser–Doppler flowmetry. CR-6 (100 mg/kg) was administered orally either at 2 and 8 h after MCA occlusion, or at 2 h only. Infarct volume, neurological deficit, and signs of reperfusion injury were evaluated. CR-6 was detected in plasma and brain by HPLC. CR-6 reduced glutathione consumption in the ischemic brain and superoxide generation in the isolated MCA. CR-6 decreased infarct volume and attenuated the neurological deficit at 1 and 7 days after ischemia/reperfusion, but not after permanent ischemia. Immediately after reperfusion, cortical blood flow values returned to their baseline (±20%) in several animals, whereas others showed hyper-perfusion (>20% of baseline). Reactive hyperemia was associated with adverse events such as increased cortical BBB leakage, edema, protein nitrotyrosination, COX-2 expression, and neutrophil accumulation; and with a poorer outcome, and CR-6 attenuated these effects. In conclusion, oral CR-6 administration after transient ischemia protects the brain from reperfusion injury.
Publisher version (URL)http://dx.doi.org/10.1038/jcbfm.2009.237
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