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[Effect of Helicobacter pylori on gastric epithelial apoptosis].

Qian Dong, Liu W, Xiao Juan ZHENG

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Abstract

To investigate the mechanisms by which Helicobacter pylori (Hp) induces gastric mucosal damage, gastric epithelial apoptotic index (AI) of normal gastric mucosa and Hp positive gastritis before and after anti-Hp treatment was studied with the method of terminal transferase mediated dUTP nick end labeling. The results showed that AI in Hp positive gastritis was higher than that in normal mucosa (P < 0.001). After the eradication of Hp, AI fell significantly to the normal level (P < 0.001). AI in persisting Hp positive gastritis had no statistically significant decrease after the anti-Hp treatment. There was no correlation between AI and the severity of gastritis. These results indicated that Hp could induce gastric epithelial apoptosis, which may be an important mechanism involved in gastric mucosal damage.

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What this paper is about

To investigate the mechanisms by which Helicobacter pylori (Hp) induces gastric mucosal damage, gastric epithelial apoptotic index (AI) of normal gastric mucosa and Hp positive gastritis before and after anti-Hp treatment was studied with the method of terminal transferase mediated dUTP nick end labeling. The results showed that AI in Hp positive gastritis was higher than that in normal mucosa (P < 0.001). After the eradication of Hp, AI fell significantly to the normal level (P < 0.001). AI in persisting Hp positive gastritis had no statistically significant decrease after the anti-Hp treatment. There was no correlation between AI and the severity of gastritis. These results indicated that Hp could induce gastric epithelial apoptosis, which may be an important mechanism involved in gastric mucosal damage.

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Available abstract

To investigate the mechanisms by which Helicobacter pylori (Hp) induces gastric mucosal damage, gastric epithelial apoptotic index (AI) of normal gastric mucosa and Hp positive gastritis before and after anti-Hp treatment was studied with the method of terminal transferase mediated dUTP nick end labeling. The results showed that AI in Hp positive gastritis was higher than that in normal mucosa (P < 0.001). After the eradication of Hp, AI fell significantly to the normal level (P < 0.001). AI in persisting Hp positive gastritis had no statistically significant decrease after the anti-Hp treatment. There was no correlation between AI and the severity of gastritis. These results indicated that Hp could induce gastric epithelial apoptosis, which may be an important mechanism involved in gastric mucosal damage.

Key concepts: Helicobacter pylori, Medicine, Gastritis, Gastric mucosa, Gastroenterology, Internal medicine, Apoptosis, Helicobacter

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