Disease relevance of Ecabet

• Efficacy of ecabet sodium enema on steroid resistant or steroid dependent ulcerative colitis [1].
• Bacterial activity of a new antiulcer agent, ecabet sodium, against Helicobacter pylori under acidic conditions [2].
• Effect of ecabet sodium enema on mildly to moderately active ulcerative proctosigmoiditis: an open-label study [3].
• Thus ecabet sodium may reduce the aggressive potential of gastric juice towards the mucosa, which may be relevant in the treatment of reflux oesophagitis and peptic ulcer disease [4].
• Efficacy and safety of ecabet sodium on functional dyspepsia: a prospective, double-blinded, randomized, multi-center controlled trial [5].

High impact information on Ecabet

• Our results suggest that ecabet may suppress TLR4-mediated inflammation or accelerated apoptosis caused H. pylori infection [6].
• In contrast, ecabet had no effect on ethanol- or etoposide-initiated apoptosis [6].
• Pretreatment with 10 mg/ml of a nonabsorbable antigastric ulcer drug, ecabet sodium (ecabet), completely blocked these two mRNA expressions and the upregulation of O2- production [6].
• Ecabet completely blocked the LPS-triggered phosphorylation of transforming growth factor-beta-activated kinase 1 (TAK1) and TAK1-binding protein 1, activation of caspase 8, loss of mitochondrial membrane potential, release of cytochrome c, activation of caspase 3, and appearance of apoptotic cells [6].
• Group LA: dual therapy (lansoprazole 30 mg o.d. plus amoxicillin 750 mg b.d.). Group LA1E: dual therapy plus ecabet sodium (1 g b.d.). Group LA2E: dual therapy plus ecabet sodium (2 g b.d.). Patients were evaluated 4 weeks after the cessation of treatment by culture and 13C-urea breath test [7].

Chemical compound and disease context of Ecabet

• High-dose ecabet sodium improves the eradication rate of helicobacter pylori in dual therapy with lansoprazole and amoxicillin [7].
• AIM: To compare ecabet sodium and cimetidine in relieving symptoms of functional dyspepsia [5].
• In vivo ecabet enema showed a therapeutic effect in the rat ulcerative colitis model induced by dextran sodium sulfate in the drinking water [8].
• In rats, ecabet sodium administration reduced the elevated activity of thymidylate synthetase in colorectal tumors [9].
• Rabeprazole, nizatidine, or ecabet sodium did not affect the severity of mucosal hyperplastic scores or histological parameters in esophagitis [10].

Biological context of Ecabet

• Inhibition of Helicobacter pylori-induced nuclear factor-kappa B activation and interleukin-8 gene expression by ecabet sodium in gastric epithelial cells [11].
• These results suggest that ecabet is bound to substrate proteins by a non-specific hydrophobic interaction to form a complex that is less vulnerable to peptic hydrolysis [12].
• A kinetic study of protein binding to ecabet sodium using quartz-crystal microbalance [13].
• The ecabet-induced increase in membrane fluidity may be involved in part in the liberation of AA from the gastric mucosal cells [14].
• Although daily treatment with ecabet sodium did not affect the colorectal DNA-synthesizing enzyme activities and bromodeoxyuridine-immunoreactive S-phase cells, high-grade dysplasia in ecabet sodium-treated mice was less frequent than in untreated mice [9].

Anatomical context of Ecabet

• Ecabet prevented both the pepsin-induced molecular size shift in mucus glycoproteins, and morphological alteration of the epithelium, including ultrastructural derangement of the mucus gel layer [15].
• However, there is little understanding of how ecabet induces anti-inflammatory activity in gastric epithelial cells infected with H. pylori [11].
• Ecabet sodium significantly inhibited pepsin activity in human gastric juice, with a maximum inhibition of 78% [4].
• The aim of this study was to examine the effects of ecabet sodium on ROS produced by human neutrophils, particularly after being primed by bacterial lipopolysaccharides (LPS) [16].
• To define the mechanism of the protection by ecabet sodium of the gastric mucosa, the characteristics of protein binding of this drug were investigated using a quartz-crystal microbalance (QCM) method [13].

Associations of Ecabet with other chemical compounds

• Incubation of H. pylori LPS with ecabet eliminated the toxic effects of the LPS, and nondenatured polyacrylamide gel electrophoresis indicated the formation of higher molecular mass complexes between H. pylori LPS and ecabet, suggesting that ecabet may interact with H. pylori LPS and block the activation of Toll-like receptor 4 (TLR4) [6].
• Relationship between gastroprotective effect of locally acting antiulcer agent ecabet sodium and its binding to gastric mucosa in rats. Comparison with sucralfate [17].
• Pepstatin significantly inhibited pepsin activity in vivo and in vitro, while ecabet Na inhibited this activity in vitro [18].
• To define the mechanism of the protection by ecabet (TA-2711) of the gastric mucosa from peptic attack, the characteristics of protein binding of this drug and its effect on peptic hydrolysis of substrate proteins were investigated in vitro [12].
• Pepstatin, ecabet Na (the anti-ulcer drug), and L-glutamine were administered intragastrically after the ligation [18].

Gene context of Ecabet

• In addition, the NF-kappa B signal inhibited by ecabet was comprised predominantly of heterodimers of p65/p50 [11].
• The ability of gastric juice to digest mucin was significantly inhibited by ecabet [4].
• Moreover, ecabet inhibited the activation of NF- kappa B and the degradation of I kappa B alpha in gastric epithelial cells in response to H. pylori infection [11].
• Effects of ecabet sodium, a novel gastroprotective agent, on mucin metabolism in rat gastric mucosa [19].
• The apparent Km values of peptic hydrolysis of BSA increased depending on the quantity of ecabet bound to BSA [12].

Analytical, diagnostic and therapeutic context of Ecabet

• 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 [11].
• Three groups of rats, i.e., a control group, esophagitis group, and an ecabet sodium group (25mg/kg given twice daily) were used [20].
• Intragastric administration of ecabet significantly increased [3H]glucosamine incorporation into antral mucin as well as into corpus mucin during five successive hours of organ culture [19].
• In pylorus-ligated rats, oral administration of cimetidine reduced gastric acid secretion, whereas ecabet did not affect the cimetidine-induced reduction in acid secretion [21].

References