Inoculation of VacA- and CagA- Helicobacter pylori delays gastric ulcer healing in the rat

Scandinavian Journal of Gastroenterology
H LiH F Helander

Abstract

Helicobacter pylori is associated with peptic ulcer disease. In the present study, the influence of VacA and CagA- H. pylori on gastric ulcer healing was studied in the rat. Twenty-four rats with acetic-acid-induced gastric ulcer were divided into two groups and given either vehicle (Brucella broth) or H. pylori suspension by gavage every 12 h for 7 days. The animals were killed 1 and 8 days after the last H. pylori gavage (i.e. 10 and 17 days after the induction of the ulcer). One hour before death, 3H-thymidine was given intraperitoneally. Tissue samples from the stomach (including the ulcer area) and the duodenum were processed for determination of labelling index and apoptotic cells. Compared with the vehicle-treated controls, the ulcer area in H. pylori-inoculated rats was significantly larger, the epithelial apoptotic cells in the ulcer margin and intact corpus were more numerous, while the cell proliferation of gastroduodenal epithelium was slightly, but not significantly, increased by H. pylori gavage. Gastric ulcer healing was delayed after the inoculation of VacA- and CagA- H. pylori in the rat, possibly as a result of excess cell loss by apoptosis.

References

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Citations

Sep 17, 2002·European Journal of Pharmacology·Peter C KonturekStanislaw J Konturek
Sep 1, 1999·The Journal of Pharmacy and Pharmacology·M SasakiiM Itoh
Apr 2, 1999·Alimentary Pharmacology & Therapeutics·P C KonturekE G Hahn
Feb 6, 2017·Disease Models & Mechanisms·Michael D BurkittD Mark Pritchard
Feb 24, 2001·The American Journal of Gastroenterology·H H Xia, N J Talley
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Sep 2, 1998·The American Journal of Physiology·S N ElliottJ L Wallace
Dec 13, 2005·Scandinavian Journal of Gastroenterology·Anders ElfvinMichael Vieth

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis