Effect of eradication of Helicobacter pylori on development and reversion of atrophic gastritis in animal study

Objective To investigate the effect of eradication of Helicobacter pylori (H.pylori) on development and reversion of atrophic gastritis by animal study. Methods One hundred and ten of two grade C 57 BL/6 female mice were randomly divided into experimental group (60 mice) and control group (50 mice). The mice in experimental group were infected with SS1 H.pylori strain, and then randomly subdivided into group A and group B, 30 mice in each group. Group A and group B received a mouse equivalent dose of standard bismuth triple therapy 6 and 12 months after infection respectively, 10 mice were subsequently sacrificed before the therapy, and 3 and 6 months after completion of the therapy, respectively, in each group. Histopathological features of the glandular stomach were graded as definiens in the Sydney System, and kinetic changes of mucosal epithelial cells of the glandular stomach were examined using anti Brdu immunohistochemical staining and flow cytometry. Results (1) H.pylori turned to negative in all mice received eradication therapy. Significant improvement of chronic active gastritis was observed after eradication of H.pylori in both group A and B, no atrophic changes was seen at any time interval in group A, whereas in group B, atrophic changes were seen 12 months after H.pylori infection and no significant change of the degree of atrophy was observed 3 and 6 months after eradication of H.pylori. (2) The cell kinetic indexes (S%, PI and LI) in the experimental group before eradication of H.pylori were significantly higher than those in the control at any time interval ( P 0.01), and significantly decreased 3 months after eradication of H.pylori compared with those before therapy ( P 0.01), and became no significant difference 6 months after eradication of H.pylori compared with those in the control at the same time intervals( P 0.05). Conclusion The study suggests that eradication of H.pylori can improve gastric mucosal inflammation and epithelial cell kinetics of the sto mach, and early treatment can prevent formation of mucosal atrophy. Once atrophy was established, eradication of H.pylori has no effects on the return to normal but may prevent its progress.