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The effect of rebamipide on the expression of proinflammatory mediators and apoptosis in human neutrophils by Helicobacter pylori water‐soluble surface proteins
Author(s) -
Kim J. S.,
Kim J. M.,
Jung H. C.,
Song I. S.
Publication year - 2003
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.18.s1.1.x
Subject(s) - rebamipide , apoptosis , secretion , helicobacter pylori , proinflammatory cytokine , chemistry , microbiology and biotechnology , immunology , medicine , pharmacology , inflammation , biology , biochemistry
Summary 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) E 2 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 PGE 2 secretion, and inhibited neutrophil apoptosis. Rebamipide suppressed PGE 2 secretion from neutrophils dose‐dependently. Rebamipide, however, did not affect neutrophil apoptosis and caspase‐3 activity. Conclusions : Rebamipide effectively suppressed PGE 2 secretion from neutrophils activated by H. pylori water‐soluble proteins. This is another possible mechanism of gastric mucosal protection by rebamipide.