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Polaprezinc Attenuates Helicobacter pylori ‐Associated Gastritis in Mongolian Gerbils
Author(s) -
Ishihara Ryu,
Iishi Hiroyasu,
Sakai Noriko,
Yano Hiroyuki,
Uedo Noriya,
Narahara Hiroyuki,
Iseki Kazushige,
Mikuni Tomiko,
Ishiguro Shingo,
Tatsuta Masaharu
Publication year - 2002
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1046/j.1523-5378.2002.00114.x
Subject(s) - helicobacter pylori , foveolar cell , gastritis , chemistry , gastroenterology , helicobacter , medicine , stomach , microbiology and biotechnology , gastric mucosa , biology
Background. The ammonia‐monochloramine system plays an important role in Helicobacter pylori ‐associated gastric mucosal injury. Polaprezinc, a new antiulcer agent, has a scavenging action against monochloramine. The aim of the experiment was to investigate the inhibitory effects of polaprezinc on the H. pylori ‐induced gastritis in Mongolian gerbils. Materials and Methods. Mongolian gerbils fasting for 24 hours were orally given culture broth containing 2–4 × 10 8 colony‐forming units of H. pylori ATCC 43054 per milliliter. From 4 hours after inoculation until the end of the experiment, gerbils were given chow pellets with or without 0.02% polaprezinc. All gerbils were killed 12 weeks later. The grades of H. pylori density and histologic features of gastritis were evaluated in accordance with the Updated Sydney System. The scavenging effect of polaprezinc on monochloramine was investigated spectrophotometrically. Results. Polaprezinc had little or no influence on the H. pylori density in both pyloric and fundic mucosae. However, it significantly attenuated the development of polymorphonuclear neutrophil activity, mononuclear infiltration, and surface epithelial erosion in both pyloric and fundic mucosae compared with those of the control group. H. pylori inoculation significantly increased the heights of both pyloric and fundic mucosae (mainly due to the increased height of foveolar hyperplasia), but polaprezinc inhibited the increase of mucosal thickness in both pyloric and fundic mucasae. No intestinal metaplasia was detected in this study. Spectrophotometric examination revealed that polaprezinc scavenged monochloramine. Conclusions. Polaprezinc inhibited the development of H. pylori ‐induced gastritis through its scavenging action against monochloramine.