Research ReportBrain infarct volume after permanent focal ischemia is not dependent on Nox2 expression

Reactive oxygen species (ROS) generated by Nox2 oxidase are reported to contribute to infarct damage following cerebral ischemia-reperfusion. Here we have examined for the first time the role of Nox2 expression in outcomes following permanent focal cerebral ischemia. Ischemia was induced by middle cerebral artery filament occlusion (MCAO) for 24 h in wild-type (WT) and Nox2−/y mice. Neurological deficit and the hanging wire test were assessed, and infarct and edema volumes were estimated using thionin-stained brain sections. Genetic deletion of Nox2 had no effect on any outcome measures at 24 h after permanent MCAO. Our data therefore suggest that ROS production by Nox2 oxidase activity plays no significant role in the pathophysiology of cerebral ischemia in the absence of reperfusion.

► Nox2 oxidase contributes to brain injury after ischemia-reperfusion. ► We tested whether Nox2 expression affects outcome at 24 h after permanent ischemia. ► In wild-type mice, NOX2 expression increased 1.8-fold after stroke. ► There was no effect of Nox2 deletion on neurological deficit or brain injury. ► Nox2 oxidase activity plays no role in outcomes of stroke without reperfusion.