Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils.
OBJECTIVE
Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacter pylori (H. pylori), no studies have been conducted regarding the effect of RPZ on gastric mucosal lesion formation caused by this bacterium. In the present study, we investigated the effect of RPZ on H. pylori-associated gastric mucosal lesion formation.


METHODS
Sixty-two male Mongolian gerbils were inoculated with H. pylori (ATCC43504) (Hp group) and 60 gerbils with the culture media alone (control group). Some gerbils in the Hp group and in the control group were injected with RPZ (1 mg/kg/day, for 7 days) at the 5th week. Gerbils were evaluated at the 12th, 24th and 48th weeks.


RESULTS
In the Hp group, all gerbils were persistently infected for 24 weeks, but 36% became negative for H. pylori at the 48th week. In the Hp + RPZ group, 18% of gerbils at the 12th week, 40% at the 24th week, and 80% at the 48th week, became negative for H. pylori. The level of neutrophil infiltration was significantly decreased in the Hp + RPZ group in comparison to the Hp group, possibly through the effects of RPZ on initial bacterial colonization and resultant inflammation. Even in the gerbils that became H. pylori-negative, the level of neutrophil infiltration was lower in the Hp + RPZ group than in the Hp group. RPZ treatment significantly increased the level of the reduced form of glutathione (GSH) at the 48th week. The elevated levels of the reduced form of GSH may have been reduced by an antioxidation process in the H. pylori-positive Hp + RPZ group.


CONCLUSIONS
Administration of RPZ not only inhibited gastric H. pylori colonization, but also reduced gastric mucosal inflammation in gerbils, possibly through its antibacterial action as well as pharmacological recruitment of the reduced form of GSH.
Suzuki
Hidekazu
H
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. hsuzuki@sc.itc.keio.ac.jp
Miyazawa
Masaharu
M
Nagahashi
Shoichi
S
Sato
Masaru
M
Bessho
Motoaki
M
Nagata
Hiroshi
H
Miura
Soichiro
S
Ishii
Hiromasa
H
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000704:Analysis of Variance; D000818:Animals; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D001562:Benzimidazoles / Q000494:pharmacology*; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000276:immunology / Q000473:pathology*; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D007249:Inflammation; D007962:Leukocytes / Q000276:immunology; D008297:Male; D009853:Omeprazole / Q000031:analogs & derivatives; D064750:Rabeprazole
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D001562:Benzimidazoles; D064750:Rabeprazole; D009853:Omeprazole