Chemopreventive effects of elm tree bark extract on Helicobacter pylori-associated mouse gastric carcinogenesis
Article first published online: 12 APR 2012
Copyright © 2012 The Korean Society for Cytopathology, The Korean Society for Legal Medicine, The Korean Society of Oral and Maxillofacial Pathology, The Korean Society of Pathologists, The Korean Society of Toxicological Pathology, The Korean Society of Veterinary Pathology and Blackwell Publishing Asia Pty Ltd
Basic and Applied Pathology
Volume 5, Issue 2, pages 31–38, June 2012
How to Cite
Kim, T.-W., Youm, S.-Y., Shin, S.-K., Kim, D. J., Hong, J. T., Kim, Y., Nam, S.-Y. and Ahn, B. (2012), Chemopreventive effects of elm tree bark extract on Helicobacter pylori-associated mouse gastric carcinogenesis. Basic and Applied Pathology, 5: 31–38. doi: 10.1111/j.1755-9294.2012.01125.x
- Issue published online: 21 JUN 2012
- Article first published online: 12 APR 2012
- Received 25 October 2011, Accepted 2 February 2012
- chronic gastritis;
- stomach neoplasms;
- intestinal metaplasia;
- Ulmus davidiana japonica.
Background and aim: Extracts of elm tree (Ulmus davidiana japonica) have long been used for the treatment of inflammatory diseases in traditional medicine. Several in vitro studies have indicated that some components of the elm tree have anti-inflammatory and/or anti-oxidative effects. We investigated the chemopreventive effects of bark extract of elm tree (BEE) on a chronic inflammation-associated mouse gastric cancer model. Methods: Gastric cancer was generated by the combination treatment of N-methyl-N-nitrosourea and Helicobacter pylori to C57BL/6 mice. Various concentrations of BEE (0, 125, 250, 500, and 1,000 ppm) was fed to the mice for 38 weeks. Results: The incidence of gastric tumors at 50 weeks were significantly lower in the highest dose BEE-fed mice (26.67%) than control mice (85.71%) (P < 0.01). The multiplicity and size of tumors were also significantly lowered by BEE feeding in a dose-dependent manner (P < 0.01). In addition, BEE decreased the nuclear β-catenin localization and nuclear cyclin-D1 expression in adenocarcinomas. Furthermore, BEE suppressed H. pylori-associated chronic inflammation determined by histologic gradings of H. pylori density, chronic gastritis, glandular atrophy and intestinal metaplasia in non-tumorous gastric mucosae. Conclusions: These findings suggest that BEE inhibits the development of gastric tumorigenesis via suppression of H. pylori infection-associated chronic inflammation.