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This study was designed to investigate the role of caspase-3/E-cadherin in  Helicobacter pylori  ( H. pylori ) -induced gastric epithelial apoptosis in cells, animal models and clinical gastritis patients. In cultured gastric mucosal epithelial cells, gastric glandular epithelial cells and C57BL/6 mice,  H. pylori  infection significantly induced apoptosis of gastric epithelial cells, down-regulated full-length E-cadherin and Bcl-2 expression, and up-regulated cleaved-caspase-3, E-cadherin/carboxy-terminal fragment 3 and Bax expression. Z-DEVD-FMK, an inhibitor of caspase-3, attenuated the effect of  H. pylori . E-cadherin overexpression significantly inhibited the apoptosis of GES-1 and SGC-7901 cells induced by the  H. pylori . The results from clinical studies also showed down-regulation of E-cadherin, up-regulation of cleaved-caspase-3 expression and increased apoptosis in gastric tissues from gastritis patients with  H. pylori  infection. These results suggest that the caspase-3/E-cadherin pathway is involved in the apoptosis of gastric epithelial cells induced by  H. pylori .

Role of caspase-3/E-cadherin in helicobacter pylori-induced apoptosis of gastric epithelial cells