In the presence of Ag(I) ions, the C-T and m(5)iC (5-methylisocytosine)-T base pairs showed comparable stability to the C-Ag(I)-C base pair, and the m(5)iC-C base pair was highly stabilized by the synergetic effect of Ag(I) coordination and possible hydrogen bonding.

Our objectives were to determine whether rebamipide, a unique antiulcer agent, would inhibit adhesive reactions between neutrophils and endothelial cells as well as the production of active oxygen species from neutrophils elicited by an extract of H. pylori. A water extract of H. pylori that was prepared from biopsy materials obtained from a patient with gastric ulcer increased the surface expression of CD18 on human neutrophils isolated from peripheral blood, the adhesion of neutrophil-endothelial cells, and the production of active oxygen species by neutrophils. Rebamipide, at concentrations of 10(-5) and 10(-6) M, reduced the adherence of neutrophils to endothelial cells as well as the CD18 expression on neutrophils induced by this bacterial extract. Rebamipide also inhibited the production of active oxygen species from neutrophils stimulated by H. pylori extract. These results suggest that rebamipide protects against the gastric mucosal inflammation associated with H. pylori by inhibiting neutrophil function.

The objectives of this study were to determine the roles of neutrophil-endothelial cell interactions and oxygen-derived free radicals in the pathogenesis of aspirin-induced gastric mucosal injury in rats. Oral administration of acidified aspirin (200 mg/kg) resulted in linear hemorrhagic erosions and an increase in myeloperoxidase activity, an index of neutrophil infiltration, in the gastric mucosa. Aspirin-induced gastric damage and the increase in myeloperoxidase activity were significantly inhibited by the injection of anti-CD11a, anti-CD11b, anti-intercellular adhesion molecule-1 monoclonal antibodies, and the combination of superoxide dismutase and catalase, which are scavengers of active oxygen species. These results suggest that neutrophil-endothelial adhesive interactions, which occur via CD11a/ CD18- and CD11b/CD18-dependent interactions with intercellular adhesion molecule-1, and oxygen-derived free radicals produced by neutrophils are implicated in the production of aspirin-induced gastric mucosal injury.

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We investigated the effect of vitamin E on gastric mucosal injury induced by Helicobacter pylori (H. pylori) infection. Male Mongolian gerbils were divided into 4 groups (normal group without H. pylori infection, vitamin E-deficient, -sufficient and -supplemented groups with H. pylori infection). Following oral inoculation with H. pylori (ATCC43504 2 x 10(8) CFU), animals were fed diets alpha-tocopherol 2 mg/100 g diet in the normal and vitamin E-sufficient groups and alpha-tocopherol 0.1 mg/100 g and 50 mg/100 g in the vitamin E-deficient and -supplemented groups, respectively, for 24 weeks. Chronic gastritis was detected in all gerbils inoculated H. pylori. Gastric ulcer was detected in 2 of 7 gerbils only in the vitamin E-deficient group. In the vitamin E-deficient group, myeloperoxidase activity and mouse keratinocyte derived chemokine (KC) in gastric mucosa was significantly higher than in the vitamin E supplemented group. Subsequently, in an in vitro study expression of CD11b/CD18 on neutrophils was enhanced by H. pylori water extract. This effect was suppressed in a dose dependent manner by the addition of alpha-tocopherol. These results suggest that vitamin E has a protective effect on gastric mucosal injury induced by H. pylori infection in gerbils, through the inhibition of accumulation of activated neutrophils.

It has been proposed that neutrophil-endothelial cell interactions mediated by adhesion molecules are involved in the pathogenesis of inflammatory bowel disease. The objective of the present study was to determine the effects of monoclonal antibodies (MAbs) directed against endothelial adhesion molecules, P-selectin and intercellular adhesion molecule-1 (ICAM-1), in rats with colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNB). Colonic inflammation was induced by administering an enema of TNB dissolved in 50% ethanol (120 mg/ml) to male Wistar rats (at a total volume of 0.25 ml per rat) after a 48-hour fast. Anti-P-selectin MAb or anti-ICAM-1 MAb was injected via the tail vein at a dose of 1 mg/kg after the induction of colitis. Rats in the control group received nonbinding mouse immunoglobulin G1. The plasma level of soluble P-selectin showed an increase within 48 h after the TNB enema. Colonic inflammation was assessed at 1 week after TNB administration. The colonic damage score and the wet weight of the colon were significantly decreased by treatment with either MAb. The increase of myeloperoxidase (MPO) activity, an index of neutrophil accumulation, and the increase of thiobarbituric acid-reactive substances (TBA-RS), an index of lipid peroxidation, in the colonic mucosa were inhibited by both MAbs. These results suggest that neutrophil-endothelial cell interactions via P-selectin and ICAM-1 play an important role in the development of TNB-induced colitis in rats.

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