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

Citation
S. Takahashi et al., Role of nuclear factor-kappa B in gastric ulcer healing in rats, AM J P-GAST, 280(6), 2001, pp. G1296-G1304
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
ISSN journal
0193-1857 → ACNP
Volume
280
Issue
6
Year of publication
2001
Pages
G1296 - G1304
Database
ISI
SICI code
0193-1857(200106)280:6<G1296:RONFBI>2.0.ZU;2-O
Abstract
We investigated the role of nuclear factor-kappaB (NF-kappaB) in gastric ul cer healing in rats. NF-kappaB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer he aling. NF-kappaB activation was observed in fibroblasts, monocytes/macropha ges, and neutrophils. Treatment of gastric fibroblasts, isolated from the u lcer base, with interleukin-1 beta activated NF-kappaB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-kappaB action resulte d in suppression of both their mRNA expression and increases in PGE(2) and CINC-1 levels induced by interleukin-1 beta. Persistent prevention of NF-ka ppaB activation caused an impairment of ulcer healing in rats. Gene express ion of interleukin-1 beta, CINC-1, cyclooxygenase-2, and inducible nitric o xide synthase in ulcerated tissue had been inhibited before the delay in ul cer healing became manifest. The increased levels of cyclooxygenase-2 prote in and PGE(2) production were also reduced. These results demonstrate that NF-kappaB, activated in ulcerated tissue, might upregulate the expression o f healing-promoting factors responsible for gastric ulcer healing in rats.