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Am J Physiol Gastrointest Liver Physiol 280: G1296-G1304, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 6, G1296-G1304, June 2001

Role of nuclear factor-kappa B in gastric ulcer healing in rats

Satoru Takahashi1,2, Takuya Fujita2, and Akira Yamamoto2

1 Department of Applied Pharmacology and 2 Department of Biopharmaceutics, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan

We investigated the role of nuclear factor-kappa B (NF-kappa B) in gastric ulcer healing in rats. NF-kappa B was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-kappa B activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1beta activated NF-kappa B and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-kappa B action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1beta . Persistent prevention of NF-kappa B activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1beta , CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-kappa B, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.

interleukin-1beta ; cytokine-induced neutrophil chemoattractant-1; cyclooxygenase-2; inducible nitric oxide synthase


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