Influence of vitamin E on gastric mucosal injury induced by Helicobacter pylori infection

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Abstract
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 × 108 CFU), animals were fed diets α‐tocopherol 2 mg/100 g diet in the normal and vitamin E‐sufficient groups and α‐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 α‐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.