| Abstract: | OBJECTIVE : To investigate the effect of eradicating Helicobacter pylori on the development and reversion of atrophic gastritis in an animal study. METHODS : One hundred and ten grade II C57BL/6 female mice were randomly divided into experimental (60 mice) and control (50 mice) groups. The mice in the experimental group were infected with the SS1 H. pylori strain, then randomly subdivided into group A and group B (30 mice in each group). Group A and group B received a dose of standard bismuth triple therapy 6 and 12 months after infection, respectively. Ten mice in each group were killed before the therapy, then at 3 and 6 months after completion of the therapy (a total of 30 mice). The histopathological features of the glandular stomach were graded using a method analogous to the Sydney system and kinetic changes in the mucosal epithelial cells of the glandular stomach were examined using anti‐BrdU immunohistochemical staining and flow cytometry. RESULTS : All mice that received eradication therapy tested negative for Helicobacter pylori. Significant improvement in chronic active gastritis was observed after the eradication of H. pylori in both groups A and B. Atrophic changes were not 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 changes in the degree of atrophy were observed 3 and 6 months after the eradication of H. pylori. The cell kinetic indices (S‐phase cell percentage, proliferation index and labeling index) in the experimental group before the eradication of H. pylori were significantly higher than those in the control group at any time (P < 0.01), and significantly decreased 3 months after the eradication of H. pylori compared with those before therapy (P < 0.01). The cell kinetic indices showed no significant difference 6 months after the eradication of H. pylori compared with those in the control group at the same time intervals (P > 0.05). CONCLUSIONS : The present study suggests that the eradication of H. pylori can reduce gastric mucosal inflammation and change the epithelial cell kinetics of the stomach. It was found that early treatment can prevent the formation of mucosal atrophy. When atrophy has established, eradication of H. pylori can no longer reverse the change but may prevent its progress. |
