In the present study, we demonstrated that ischemic postconditioning inhibited the ischemia/reperfusion-induced higher level of phosphorylated NF-κB/p65 in both cytoplasm and nucleus, which was consistent with the finding that ischemic postconditioning reversed the decreased level of IκBα caused by cerebral ischemia/reperfusion (figure 4). Here, NFKB1 is linked to brain ischemia.