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  • 1
    ISSN: 1523-5378
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background.  Helicobacter pylori stimulates nuclear factor-kappa B (NF-κB) activation and chemokine interleukin-8 (IL-8) expression in gastric epithelial cells. Ecabet sodium (ecabet), a locally acting antiulcer drug, is known to have anti-H. pylori activity. However, there is little understanding of how ecabet induces anti-inflammatory activity in gastric epithelial cells infected with H. pylori. The aim of this study was to investigate the effects of ecabet on IL-8 gene expression and NF-κB activation in human gastric epithelial cells infected with H. pylori.Materials and Methods.  After Hs746T, MKN-45, or SNU-5 gastric epithelial cell lines had been infected with cagA+cytotoxin+H. pylori in the presence of ecabet, IL-8 mRNA expression was assessed by quantitative reverse transcription–polymerase chain reaction, and IL-8 secretion was measured by enzyme-linked immunosorbent assay. NF-κB and inhibitory kappa B-alpha (IκBα) signals were assayed by electrophoretic mobility shift assay and Western blot, respectively. The activation of NF-κB and IL-8 reporter genes was determined by luciferase assay.Results.  Ecabet showed no antimicrobial activiy against Gram-positive or -negative bacteria. However, ecabet inhibited transcription of the IL-8 gene and secretion of IL-8 by gastric epithelial cells infected with H. pylori at a concentration of 5 µg/ml. Moreover, ecabet inhibited the activation of NF-κB and the degradation of IκBα in gastric epithelial cells in response to H. pylori infection. In addition, the NF-κB signal inhibited by ecabet was comprised predominantly of heterodimers of p65/p50.Conclusions.  Ecabet inhibited H. pylori-induced IL-8 gene transcription and secretion by suppressing the NF-κB signal. This inhibition might be one pathway by which ecabet exerts its anti-inflammatory effect on H. pylori-induced gastric inflammation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: Helicobacter pylori ; intestinal metaplasia ; eradication ; duodenal ulcer ; gastric ulcer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was conducted to investigate whether or not the eradication of H. pylori could lead to the regression of intestinal metaplasia (IM) in patients with either duodenal ulcer (DU) or benign gastric ulcer (BGU). The initial antral IM grade was 0.21 in the 72 patients of the H. pylori-eradicated DU group, this decreased to 0.17, 0.14, 0.13, and 0.09 after periods of four weeks, one year, two years, and four years, respectively, but without statistical significance. In the corpus of the DU group, where IM grade was low (0.02), there was no detectable change in IM. The initial antral IM grade of 0.69 in the 41 patients of the H. pylori-eradicated BGU group decreased substantially to 0.61, 0.44, and 0.39 after periods of four weeks and one and two years, respectively, but again without statistical significance. The initial corporal IM grade of the BGU group of 0.27 decreased to 0.20, 0.15, and 0.06 after periods of four weeks and one and two years, again without statistical significance. In contrast, the IM grades of the noneradicated DU group (N = 20) and the BGU group (N = 16) showed nearly no change in the antrum and corpus. Gastritis grades of antrum and corpus in the H. pylori-eradicated DU or BGU group significantly decreased with respect to time (P = 0.0001), but there were no significant changes in the corresponding noneradicated groups. Although there was no statistical significance, IM decreased in the antrum and corpus of the stomach with BGU and in antrum of those with DU over a two to four-year period after H. pylori eradication, suggesting the possible reversibility of IM.
    Type of Medium: Electronic Resource
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