It is well established that TNF-α is one of the major stimuli toward phosphorylation of NF-κB. To confirm TNF-α-mediated signaling following SE, we performed an immunohistochemical study using five phospho-NF-κB antibodies. Compared to non-SE animals (data not shown), 12 hr-post SE animals of the saline-infused group showed p65-Ser276, p65-Ser311, p65-Ser529, and p65-Ser536 phosphorylation in astrocytes (not endothelial cells). sTNFp55R infusion effectively reduced p65-Ser276 and p65-Ser311 phosphorylation (p < 0.05, respectively), while it could not affect p65-Ser529 or p65-Ser536 phosphorylation (Figures 3 and 4A). In contrast, p65-Thr435 phosphorylation was increased in endothelial cells (not astrocytes) within the PC of saline-infused animals 12 hr after SE (Figure 5A). In addition, sTNFp55R infusion effectively alleviated SE-induced p65-Thr435 phosphorylation in endothelial cells, compared to saline infusion (p < 0.05, Figure 5B).