[Effects of Helicobacter pylori, omeprazole and gastrin on the proliferation and apoptosis of gastric epithelial cell].

OBJECTIVE

to explore whether there is an interaction between Helicobacter pylori (H. pylori), omeprazole and gastrin on the proliferation and apoptosis of gastric epithelial cells.

METHODS

With omeprazole, H. pylori and gastrin as treatment factors, the in vitro changes of gastric epithelial cells AGS and GES-1 were detected by MTS, Hoechst33342 and flow cytometry.

RESULTS

(1) for a single factor, the gastric mucosal cells (AGS and GES-1) treated by H. pylori or omeprazole show significantly higher apoptosis than that of control group [H. pylori and 104 nmol/L omeprazole group: (17.20 ± 0.90)%, (12.81 ± 0.78)% vs (7.96 ± 1.25)%; (4.60 ± 0.34)%, (6.60 ± 0.76)% vs (3.52 ± 0.16)%; all P < 0.05]. The gastric mucosal cells treated by H. pylori or omeprazole show significantly lower proliferation than that of control group (H. pylori and 104 nmol/L omeprazole group: 13.35 ± 0.55 vs 37.78 ± 1.98, 47.62 ± 2.40 vs 62.44 ± 4.46; 27.15 ± 1.64 vs 32.76 ± 1.57, 29.42 ± 1.44 vs 48.86 ± 4.95; all P < 0.05). The differences were statistically significant and the effects were correlated with the concentration of omeprazole. Gastrin had no direct effect on cellular proliferation and apoptosis (all P > 0.05). (2) For a combinations of factors, the GES-1 cells treated with H. pylori and 500 ng/L gastrin had a significantly higher ratio [(7.25 ± 0.54)% vs (4.60 ± 0.34)%, P < 0.05], while the other groups just showed a rising trend in the proportion of apoptosis cells, but there was no statistical significance. Flow cytometry analysis showed that combinations of H. pylori, omeprazole and gastrin caused lower proliferation than that of H. pylori group, and all changes were statistically significant (AGS: 12.68 ± 0.09, 12.28 ± 0.31 vs 13.35 ± 0.55; GES-1: 22.06 ± 1.61, 18.59 ± 0.09 vs 27.15 ± 1.64; all P < 0.05). And combinations of 104 nmol/L omeprazole and 500 ng/L gastrin caused lower proliferation than that of 104 nmol/L omeprazole group (33.23 ± 5.98 vs 47.62 ± 2.40 and 25.97 ± 0.74 vs 29.42 ± 1.44, both P < 0.05). (3) When comparing the apoptosis and proliferation changes of two cell lines, gastric cancer cells AGS had a more marked changes than immortalized cells GES-1.

CONCLUSION

gastrin significantly enhances the effects of omeprazole and H. pylori on gastric epithelial cells. It is speculated that the factors of omeprazole, H. pylori and gastrin may have a synergistic effect of decreased proliferation and increased apoptosis of gastric mucosal cells. Thus a long-term proton pump inhibitor treatment of H. pylori patients may carry a higher risk of atrophic gastritis. But it needs to be confirmed by further experiments.