Combined effect of rebamipide and ecabet sodium on Helicobacter pylori adhesion to gastric epithelial cells

Helicobacter pylori is a major etiological agent in gastroduodenal disorder s. The adhesion of H, pylori to gastric epithelial cells is the initial ste p of N, pylori infection. Inhibition of H, pylori adhesion is thus a therap eutic target in the prevention of H, pylori infection. me have reported tha t rebamipide and ecabet sodium, mucoprotective antiulcer agents, independen tly inhibit H. pylori adhesion. However, the antiadhesion activity of each antiulcer agent was incomplete. Experiments were performed to evaluate the combined effect of rebamipide and ecabet sodium on H, pylori adhesion to ga stric epithelial cells, MKN-28 and MKN-45 cells, derived from human gastric carcinomas, were used as target cells, Twelve clinical isolates of H, pylo ri were used in this study. We evaluated the effects of rebamipide and ecab et sodium, individually and in combination, on H. pylori adhesion to target cells quantitatively using our previously established enzyme-linked immuno sorbent assay. Rebamipide and ecabet sodium each partially inhibited H. pyl ori adhesion. In contrast, adhesion was almost completely inhibited by pret reating target cells and N, pylori with the combination of rebamipide and e cabet sodium, Our studies suggest that the synergistic antiadhesion activit y of rebamipide and ecabet sodium is greater than that of each antiulcer ag ent alone.