Korean J Gastroenterol.
2002 Jan;39(1):13-21.
Effect of Rebamipide on the Neutrophils Activated by Helicobacter pylori Water-Soluble Proteins
- Affiliations
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- 1Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, hyunchae@plaza.snu.ac.kr
- 2Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
Abstract
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Background/Aims: Helicobacter pylori (H. pylori) infection induces persistent neutrophil infiltration in gastric mucosa. The expression of cyclooxygenase (COX)-2 and inhibition of apoptosis in the neutrophils could contribute to the pathogenesis of H. pylori infection. Rebamipide, a mucosal protective and ulcer-healing drug, has been known to inhibit neutrophil activation. The aim of this study was to evaluate the effect of rebamipide on the neutrophils activated by Helicobacter pylori water-soluble proteins.
Methods
After neutrophils were stimulated with H. pylori water extract (HPWE) or pretreated with rebamipide, the expression of COX-2 mRNA and protein was assessed by quantitative RT-PCR and Western blotting, respectively. Prostaglandin (PG) E2 synthesis was determined by radioimmunoassay. Neutrophil apoptosis was evaluated by cytosolic oligonucleosome-bound DNA ELISA and caspase-3 activity was measured by the detection of p-nitroanilide after cleavage from labeled substrate.
Results
Stimulation with HPWE upregulated COX-2 expression and PGE2 secretion, and inhibited neutrophil apoptosis. Rebamipide suppressed PGE2 secretion from neutrophils in a dose-dependent manner. However, rebamipide did not affect neutrophil apoptosis and caspase-3 activity.
Conclusions
Rebamipide effectively suppresses PGE2 secretion from neutrophils activated by H. pylori water-soluble proteins. This is another possible mechanism of gastric mucosal protection by rebamipide.