ArticleDigestive diseases and sciences2010
Gastritis induced by Helicobacter pylori infection in experimental rats.
Article in Digestive diseases and sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- A novel cycloastragenol-encapsulated carboxymethyl chitosan-silk fibroin hydrogel combined with sucralfate alleviates MNNG-induced chronic atrophic gastritis by targeting HIF-1α and VEGF signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Integrated analysis of myeloperoxidase in gastric health and cancer: associations with pepsinogen levels, immune regulation, and prognosis in a large healthy population-based and TCGA cohorts.Frontiers in immunology · 2025Article
- Research advances of the establishment and characterization ofFrontiers in microbiology · 2025Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastritis, an inflammation of gastric mucosa, may be due to many pathological factors and infection, such as with Helicobacter pylori. The use of experimental models of gastritis is important to evaluate the biochemical changes and study chemotherapeutic intervention. In a previous study we demonstrated an acute gastritis model induced by iodoacetamide.
aimsOur objective in this study was to evaluate a new gastritis model induced by H. pylori infection in experimental rats in terms of certain biomarkers in serum and mucosal tissues in addition to histopathological examination.
methodsGastritis was induced in 20 albino Wistar rats by H. pylori isolated from antral biopsy taken from a 49-year-old male patient endoscopically diagnosed as having H. pylori infection. Another ten rats were used as controls. Serum gastrin, pepsinogen I activity, interleukin-6 (IL-6) and gastric mucosal myeloperoxidase (MPO) activity and prostaglandin E(2) (PGE(2)) were measured. Immunostaining for inducible nitric oxide synthase (iNOS), nitrotyrosine and DNA fragmentation were used to further evaluate H. pylori-induced gastritis.
resultsSerum gastrin, IL-6, mucosal MPO activity, and PGE(2) demonstrated significant increases joined with a decreased serum pepsinogen I activity (P < 0.001). Immunohistochemistry demonstrated positive reaction for iNOS, nitrotyrosine and DNA fragmentation.
conclusionsHelicobacter pylori-induced gastritis models demonstrated massive oxidative stress and pronounced injury in mucosal tissue. Since our model in rats reflected the clinical picture of H. pylori infection, it can be considered as a consistent model to study chemotherapeutic intervention for this type of gastritis.
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