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. 2008 Feb 24;99(5):836–842. doi: 10.1111/j.1349-7006.2008.00763.x

Figure 3.

Figure 3

Participation of the nuclear factor‐kappaB (NF‐κB) activation in the Helicobacter pylori (H. pylori) infection and dextran sulfate sodium salt (DSS) colitis models. (a) Hematoxylin–eosin (HE) and phospho‐IκBα stainings of the antrum part 25 weeks after H. pylori infection are shown. By the infection of cag PAI‐negative H. pylori (Δcag) without the activation ability of NF‐κB, degree of the chronic gastritis and phospho‐IκBα staining are extremely slight in comparison with the infection of the wild‐type (WT) (magnification 40 ×). (b) Hematoxylin–eosin (HE) and phospho‐IκBα stainings of the colonic part 10 days after DSS administration are shown. By the treatment of NF‐κB essential modulator (NEMO)‐binding domain (NBD) peptides which inhibit NF‐κB activity, degree of the colitis and phospho‐IκBα staining are extremely slight compared with the absence of NBD peptides (magnification 10 × in HE and 40 × in phospho‐IκBα staining).