Abstract
Since the discovery of Helicobacter pylori (H. pylori), many efforts have been made to establish animal models for the investigation of the pathological features and molecular mechanisms of gastric carcinogenesis. Among the animal models, Mongolian gerbils and mice are particularly useful for the analysis of H. pylori-associated inflammatory reactions and gastric cancer development. Inhibitors of oxidative stress, cyclooxygenase-2 (COX-2) and nuclear factor-κB, exert preventive effects on chronic gastritis and the development of adenocarcinomas in H. pylori-infected gerbils. Genetically-modified mouse models, including transgenic and knockout mice, have also revealed the importance of p53, COX-2/prostaglandin, Wnt/β-catenin, proinflammatory cytokines, gastrin and type III mucin in the molecular mechanisms of gastric carcinogenesis. Microarray technology is available for comprehensive gene analysis in the gastric mucosa of mouse models, and epigenetics, such as DNA methylation, could be an alternative approach to correlate the observations in animal models with the etiology in humans.
Highlights
Gastric cancer is the fourth most common cancer and second leading cause of cancer-related death in the world [1]
COX-2 has been shown to be involved in the processes of inflammation and carcinogenesis [56], and previous studies indicate that COX-2 expression is associated with H. pylori-induced gastritis and stomach carcinogenesis in humans [57,58]
MRNA expression of inflammatory factors, such as tumor necrosis factor-α (Tnf-α), interferon-γ, interleukin (Il)-2, Il-6, KC (Il-8 homologue) and iNos, was significantly decreased in the pyloric mucosa. These results indicate that Caffeic acid phenethyl ester (CAPE) has inhibitory effects on H. pylori-induced gastritis in gerbils through the suppression of Nuclear factor-κB (NF-κB) activation and may have the potential for the prevention and therapy of H. pylori-associated gastric disorders [74]
Summary
Gastric cancer is the fourth most common cancer and second leading cause of cancer-related death in the world [1]. Since Helicobacter pylori (H. pylori) was discovered about 30 years ago [2,3], a lot of epidemiological and experimental studies have revealed a significant relationship between H. pylori infection and chronic/atrophic gastritis, peptic ulcer, intestinal metaplasia, gastric lymphoma or cancer development [4,5,6,7,8,9,10,11,12,13,14]. Many experimental studies have been performed to investigate the mechanisms of gastric carcinogenesis using animal models, as well as clinical samples. Mongolian gerbils and mice are useful for the analysis of H. pylori-associated gastric disorders [17,18]. We will review the research to date for the analysis of the molecular mechanisms of H. pylori-associated gastric carcinogenesis using rodent models
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