The effect of rebamipide on the expression of proinflammatory mediators and apoptosis in human neutrophils by Helicobacter pylori water-soluble surface proteins.

Abstract:

BACKGROUND:Helicobacter pylori infection elicits 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. AIM:To evaluate the effect of rebamipide on the neutrophils activated by H. pylori water-soluble proteins. METHODS:After neutrophils were stimulated with H. pylori water extract (HPWE) or pre-treated 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 labelled substrate. RESULTS:Stimulation with HPWE up-regulated COX-2 expression and PGE2 secretion, and inhibited neutrophil apoptosis. Rebamipide suppressed PGE2 secretion from neutrophils dose-dependently. Rebamipide, however, did not affect neutrophil apoptosis and caspase-3 activity. CONCLUSIONS:Rebamipide effectively suppressed PGE2 secretion from neutrophils activated by H. pylori water-soluble proteins. This is another possible mechanism of gastric mucosal protection by rebamipide.

journal_name

Aliment Pharmacol Ther

authors

Kim JS,Kim JM,Jung HC,Song IS

doi

10.1046/j.1365-2036.18.s1.1.x

subject

Has Abstract

pub_date

2003-07-01 00:00:00

pages

45-54

eissn

0269-2813

issn

1365-2036

pii

1502

journal_volume

18 Suppl 1

pub_type

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