Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils

Hidekazu Suzuki, Masaharu Miyazawa, Shoichi Nagahashi, Masaru Sato, Motoaki Bessho, Hiroshi Nagata, Soichiro Miura, Hiromasa Ishii

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background and Aim: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacterpylori (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. Conclusion: 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.

Original languageEnglish
Pages (from-to)787-795
Number of pages9
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume18
Issue number7
DOIs
Publication statusPublished - 2003 Jul 1

Fingerprint

Rabeprazole
Gerbillinae
Helicobacter pylori
Stomach
Neutrophil Infiltration
Inflammation
Control Groups
Proton Pump Inhibitors
Glutathione
Culture Media

Keywords

  • Antioxidant
  • Gastritis
  • Helicobacter pylori
  • Leukocyte
  • Oxygen radical
  • Proton pump inhibitor

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils. / Suzuki, Hidekazu; Miyazawa, Masaharu; Nagahashi, Shoichi; Sato, Masaru; Bessho, Motoaki; Nagata, Hiroshi; Miura, Soichiro; Ishii, Hiromasa.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 18, No. 7, 01.07.2003, p. 787-795.

Research output: Contribution to journalArticle

Suzuki, Hidekazu ; Miyazawa, Masaharu ; Nagahashi, Shoichi ; Sato, Masaru ; Bessho, Motoaki ; Nagata, Hiroshi ; Miura, Soichiro ; Ishii, Hiromasa. / Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils. In: Journal of Gastroenterology and Hepatology (Australia). 2003 ; Vol. 18, No. 7. pp. 787-795.
@article{85f32cc415ce43ecb3c676688a49eb87,
title = "Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils",
abstract = "Background and Aim: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacterpylori (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. Conclusion: 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.",
keywords = "Antioxidant, Gastritis, Helicobacter pylori, Leukocyte, Oxygen radical, Proton pump inhibitor",
author = "Hidekazu Suzuki and Masaharu Miyazawa and Shoichi Nagahashi and Masaru Sato and Motoaki Bessho and Hiroshi Nagata and Soichiro Miura and Hiromasa Ishii",
year = "2003",
month = "7",
day = "1",
doi = "10.1046/j.1440-1746.2003.03038.x",
language = "English",
volume = "18",
pages = "787--795",
journal = "Journal of Gastroenterology and Hepatology (Australia)",
issn = "0815-9319",
publisher = "Wiley-Blackwell",
number = "7",

}

TY - JOUR

T1 - Rabeprazole treatment attenuated Helicobacter pylori-associated gastric mucosal lesion formation in Mongolian gerbils

AU - Suzuki, Hidekazu

AU - Miyazawa, Masaharu

AU - Nagahashi, Shoichi

AU - Sato, Masaru

AU - Bessho, Motoaki

AU - Nagata, Hiroshi

AU - Miura, Soichiro

AU - Ishii, Hiromasa

PY - 2003/7/1

Y1 - 2003/7/1

N2 - Background and Aim: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacterpylori (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. Conclusion: 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.

AB - Background and Aim: Although rabeprazole (RPZ), a proton pump inhibitor, has been reported to have a bactericidal effect on Helicobacterpylori (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. Conclusion: 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.

KW - Antioxidant

KW - Gastritis

KW - Helicobacter pylori

KW - Leukocyte

KW - Oxygen radical

KW - Proton pump inhibitor

UR - http://www.scopus.com/inward/record.url?scp=0042703459&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042703459&partnerID=8YFLogxK

U2 - 10.1046/j.1440-1746.2003.03038.x

DO - 10.1046/j.1440-1746.2003.03038.x

M3 - Article

C2 - 12795750

AN - SCOPUS:0042703459

VL - 18

SP - 787

EP - 795

JO - Journal of Gastroenterology and Hepatology (Australia)

JF - Journal of Gastroenterology and Hepatology (Australia)

SN - 0815-9319

IS - 7

ER -