Platelet-activating factor modulates gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide
Section snippets
Materials and methods
Animals. The study was conducted with Sprague–Dawley rats in compliance with the Institutional Animal Care and Use Committee. The animals were divided into groups and subjected to two different types of treatment regimen. In one, prophylactic, the animals at 16 and 4 h, before intragastric surface epithelial application of H. pylori LPS at 50 μg/animal [3], [7], were administered at 0–30 mg/kg with BN52020 (Calbiochem) or vehicle consisting of 5% gum arabic in saline, whereas in the second type of
Results
The role of PAF as a mediator of gastric mucosal inflammatory reaction to H. pylori infection and the underlying mechanism of its action were assessed in the animal model of H. pylori LPS-induced gastritis using rats subjected to intragastric administration of a specific PAF antagonist, BN52020, either before (prophylactic) or after (therapeutic) the LPS application. The results of histologic examination of the mucosa 4 days after exposure of the animals to the LPS in the absence of BN52020
Discussion
Enhancement in gastric mucosal TNF-α production, excessive NO and prostaglandin generation, and alteration in the extent of epithelial cell apoptosis are well-recognized features of gastritis associated with H. pylori infection in humans as well as characterize mucosal inflammatory responses in the animal model of H. pylori LPS-induced gastritis [3], [4], [9]. Studies indicate that up-regulation in NO and prostaglandins with H. pylori infection is the result of TNF-α-mediated activation of the
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