gms | German Medical Science

27. Deutscher Krebskongress

Deutsche Krebsgesellschaft e. V.

22. - 26.03.2006, Berlin

Effect of probiotics and triple eradication therapy on the cyclooxygenase (COX)-2 expression, apoptosis and functional gastric impairment in the animal model of Helicobacter pylori-induced carcinogenesis

Meeting Abstract

  • corresponding author presenting/speaker Peter C. Konturek - Medizinische Klinik 1, Universität Erlangen-Nürnberg, Deutschland
  • Tomasz Brzozowski - Institut für Physiologie, Universität Krakau
  • Stanislaw Konturek - Institut für Physiologie, Universität Krakau
  • Jerzy Stachura - Institut für Physiologie, Universität Krakau
  • Eckhart G. Hahn - Medizinische Klinik 1, Universität Erlangen-Nürnberg

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocPO181

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Veröffentlicht: 20. März 2006

© 2006 Konturek et al.
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Background: H. pylori infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis which mimics H. pylori-positive patients developing gastric ulcer and gastric cancer, but effect of probiotic therapy on functional aspects of this infection remains unknown.

Methods: We compared the effects of intragastric (i.g.) inoculation of gerbils with H. pylori strain (cagA+ vacA+, 5x106 CFU/ml) with or without triple therapy including omeprazole, amoxicillin and tinidazol or probiotic bacteria Lacidofil. Histology of glandular mucosa, the viable H. pylori and density of H. pylori-colonization were evaluated. The gastric blood flow (GBF) was measured by H2-gas clearance method; the plasma gastrin and gastric luminal somatostatin were determined by RIA and expression of COX-2 and apoptotic Bax and Bcl-2 proteins were evaluated by Western Blot.

Results: The gastric H. pylori infection was detected in all animals by histology and H. pylori culture. Basal gastric acid was significantly reduced in H. pylori-infected animals but not in those with triple therapy or Lacidofil. Early lesions were seen already 4 weeks upon H. pylori-inoculation and consisted of chronic gastritis and glandular atypia associated with typical regenerative hyperplasia and increased mitotic activity and formation of apoptotic bodies. The H. pylori-infection was accompanied by the fall in GBF, the marked increase in plasma gastrin, the significant fall in gastric somatostatin levels and Bcl-2 protein expression and the rise in expression of COX-2 and Bax proteins. These mucosal changes were counteracted by the triple therapy and Lacidofil.

Conclusions: H. pylori-infection in gerbils, associated with regenerative hyperplasia of glandular structure, results in the suppression of gastric secretion, overexpression of COX-2 and enhancement in apoptosis and impairment of both, GBF and gastrin-somatostatin link which were reversed by anti- H. pylori triple therapy and attenuated by probiotics.