Role of endothelin-1 and constitutive nitric oxide synthase in gastric mucosal resistance to indomethacin injury: effect of antiulcer agents.

@article{Slomiany1999RoleOE,
  title={Role of endothelin-1 and constitutive nitric oxide synthase in gastric mucosal resistance to indomethacin injury: effect of antiulcer agents.},
  author={Bronislaw L. Slomiany and Jerzy K. Piotrowski and Amalia Slomiany},
  journal={Scandinavian journal of gastroenterology},
  year={1999},
  volume={34 5},
  pages={
          459-64
        }
}
BACKGROUND Endothelin-1 (ET-1) and nitric oxide, recognized key mediators implicated in the pathophysiology of gastric mucosal injury, are known to exert opposing effects on the inflammatory processes mediated by regulatory cytokines. In this study we investigated the mucosal expression of ET-1 and interleukin-4 (IL-4) and the activity of constitutive nitric oxide synthase (cNOS) during indomethacin-induced gastric mucosal injury and evaluated the effect of antiulcer agents, omeprazole and… 
Role of Endothelin-converting Enzyme-1 in the Suppression of Constitutive Nitric Oxide Synthase in Rat Gastric Mucosal Injury by Indomethacin
Background: Disturbances in nitric oxide generation and the release of a vasoactive peptide, endothelin-1 (ET-1), are well recognized early events in pathogenesis of NSAID-induced gastropathy. In
Suppression of endothelin-converting enzyme-1 by sucralfate, a factor in gastric mucosal resistance to indomethacin injury in rats
TLDR
It is demonstrated that gastric mucosal injury by indomethacin is associated with up-regulation of ECE-1 expression, which leads to the enhancement of ET-1 production, induction of TNF-α, and triggering of apoptotic events that exacerbate the inflammatory process.
Involvement of interleukin-4 in down-regulation of endothelin-1 during gastric ulcer healing: Effect of ebrotidine
TLDR
It is suggested that a drop in the mucosal expression of IL-4 at the ulcer onset causes dysregulation of ET-1 production, induction of TNF-α and triggers the apoptotic events that affect the efficiency of the repair process.
Endothelin-1, inducible nitric oxide synthase and macrophage inflammatory protein-1alpha in the pathogenesis of stress ulcer in neurotraumatic patients.
TLDR
Prophylactic OME is effective in reducing the severity of stress ulcerations in severe neurotraumatic patients and fails to counter the enhancement in the mucosal expression of ET-1, iNOS, and MIP-1alpha caused by severe brain damage.
Endothelin-1-dependent up-regulation of leptin production in gastric mucosal injury by indomethacin
TLDR
The results implicate endothelin-1 as a key factor in the regulation of leptin production associated with gastric mucosal response to injury, and show that the stimulatory effect of ET-1 on leptin production occurs via ETA receptor activation.
Role of prostaglandins and nitric oxide in gastric damage induced by metamizol in rats
TLDR
In addition to inhibition of PG synthesis, damage induced by metamizol was associated with an inhibition of the NO/cGMP pathway and cNOS activity, and diclofenac-induced gastric damage wasassociated with an increase of the inflammatory response.
Up-regulation in endothelin-1 by Helicobacter pylori lipopolysaccharide interferes with gastric mucin synthesis via epidermal growth factor receptor transactivation
TLDR
These findings are the first to show that the detrimental effect of H. pylori on gastric mucin synthesis is intimately linked to the events associated with ECE-1 up-regulation, enhancement in ET-1 production, and G protein-coupled ETA receptor activation that triggers the EGFR transactivation.
Effect of ebrotidine on Helicobacter pylori lipopolysaccharide-induced up-regulation of endothelin-1 in gastric mucosa
TLDR
It is shown that ebrotidine is capable of suppressing the H. pylori-induced gastric mucosal inflammatory responses by analyzing over a period of 10 days the extent of epithelial cell apoptosis and the mucosal expression of endothelin-1, tumor necrosis factor α, and the activity of constitutive (cNOS) and inducible (NOS-2) nitric oxide synthase.
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