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Background and Purpose— We have previously identified an increased susceptibility of Gpx1−/− mice to increased infarct size after middle cerebral artery occlusion (MCAO). This study was designed to elucidate the mechanisms involved in elevated neuronal cell death arising from an altered endogenous oxidant state.Methods— Gpx1−/− mice were exposed to transient MCAO and reperfusion by intraluminal suture blockade. Protein expression of the p65 subunit of transcription factor nuclear factor-κB (NF-κB) was examined by immunohistochemistry and Western Analysis. NF-κB DNA-protein activity was assessed by electrophoretic mobility shift assays (EMSA). Wild-type and Gpx1−/− mice were exposed to MCAO with or without the NF-κB inhibitor, pyrrolidinedithiocarbamate (PDTC).Results— Upregulation of the p65 subunit of NF-κB and subsequent p65 phosphorylation at serine 536 was detected in the Gpx1−/− brains after stroke. EMSAs revealed that increased ischemia-enhanced DNA binding of NF-κB was observed in Gpx1−/− mice compared with wild-type. Supershift assays indicated that the p50 and p65 subunits participated in the bound NF-κB complex. The NF-κB inhibitor PDTC, a potential antioxidant, was able to afford partial neuroprotection in the Gpx1−/− mice.Conclusions— NF-κB is upregulated in the Gpx1−/− mouse, and this upregulation contributes to the increased cell death seen in the Gpx1−/− after MCAO. The activation of NF-κB may increase the expression of downstream target genes that are involved in the progression of neural injury after MCAO.

Potential Contribution of NF-κB in Neuronal Cell Death in the Glutathione Peroxidase-1 Knockout Mouse in Response to Ischemia-Reperfusion Injury