[Acetic acid-induced gastro-duodenal ulcers in experimental animals--examples of serendipity and pseudoserendipity].
Our understanding of the function and etiology of various gastric diseases has exponentially expanded over the past 40 years. In particular, several animal models had been devised and used for screening of anti-ulcer drugs and elucidation of pathogenesis. This review describes how water-immersion stress ulcer model, Helicobacter pylori ulcer model, and acetic acid ulcer models were established in experimental animals. In recent years, genetically modified mice allowed rapid accumulation of very important findings. H(2)-receptor knockout mice revealed to exhibit Menetrier's disease-like gastric mucosal changes. Gastrin-transgenic mice infected with H. pylori revealed to develop gastric cancer. The hypothesis for the origin of parietal cells was provided.
Okabe
Susumu
S
Kyoto Pharmaceutical University, Kyoto 607-8414, Japan. sokabe@dwc.doshisha.ac.jp
D000085:Acetates / Q000009:adverse effects*; D000818:Animals; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000166:cytology / Q000378:metabolism; D005755:Gastrins / Q000235:genetics; D005758:Gastritis, Hypertrophic / Q000209:etiology; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D006801:Humans; D007101:Immersion / Q000009:adverse effects; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D051381:Rats; D011970:Receptors, Histamine H2 / Q000235:genetics; D013276:Stomach Ulcer / Q000209:etiology*; D013312:Stress, Physiological / Q000150:complications
D000085:Acetates; D005755:Gastrins; D011970:Receptors, Histamine H2