The effect of rebamipide on cellular release of leukotriene B4 by Helicobacter pylori.
- Author:
Jung Jin LEE
1
;
Bok Gee HAN
;
Jai Youl RO
;
Kwang Ho RHEE
;
Hee Shang YOUN
;
Mal Nam KIM
;
Myung Hee CHUNG
Author Information
1. Department of Biology, Sangmyung University, Seoul 110-799 South Korea.
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
Leukotriene B4;
Rebamipide
- MeSH:
Adenoma;
Calcimycin;
Gastritis;
Helicobacter pylori*;
Helicobacter*;
Humans;
Inflammation;
Leukotriene B4*;
Leukotrienes;
Neutrophils;
Peptic Ulcer;
Stomach Ulcer
- From:The Korean Journal of Physiology and Pharmacology
1997;1(6):825-830
- CountryRepublic of Korea
- Language:English
-
Abstract:
Leukotrienes (LTs) are known to act as a mediator provoking tissue response in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H. pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer, but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study, this possibility was tested using LTB4 as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of LTB4 from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of LTB4 was induced by neutrophils and Kato III cells when these cells incubated with H. pylori 4.8 X 108 cells/ml for 30 min. But in the presence of rebamipide the release of LTB4 from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells, respectively. We also obtained the results that the release of LTB4 was induced by A23187 (Ca2+ ionophore) and the A23187-induced release was also inhibited by rebamipide. It seems that the mechanism of action of rebamipide is through its interaction with the level of intracellular Ca2+. In view of the roles of LTB4 in inflammatory reaction and the roles of H. pylori in gastritis and peptic ulcer, the effects of this drug observed in this study may contribute to their therapeutic action in these gastric disorders.
