Effect of Helicobacterpyloriinfection on Bax protein expression in patients with gastric precancerous lesions

AIM: To investigate the effect of Helicobacter pylori (H pylori) infection on Bax protein expression, and explore the role of H pylori in gastric carcinogenesis.METHODS: H pylori was assessed by rapid urease test and Warthin-Starry method, and expression of Bax protein was examined immunohistochemically in 72 patients with pre-malignant lesions.RESULTS: Bax protein was differently expressed in intestinal metaplasia and gastric dysplasia, and showed 63.99% positivity. The positivity of Bax protein expression in H pylori-positive gastric precancerous lesions (72.3%) was significantly higher than that in H pylori-negative gastric precancerous lesions (48.0%, χ2 = 4.191, P＜0.05).H pylori infection was well correlated with the expression of Bax protein in gastric precancerous lesions (r = 0.978,P＜0.01). After eradication of H pylori, the positivity of Bax protein expression significantly decreased in H pylori-positive gastric precancerous lesions (χ2= 5.506,P＜0.05). In the persisting H pylori-infected patients,the positivity of Bax protein expression was not changed.CONCLUSION: H pylori infection may be involved in the upregulation of Bax gene, which might be one of the mechanisms of H pylori infection-induced gastric epithelial cell apoptosis. H pylori might act as a tumor promoter in the genesis of gastric carcinoma and eradication of H pylori could inhibit gastric carcinogenesis.

AIM： To investigate the effect of Helicobacter pylori （H pylon） infection on Bax protein expression, and explore the role of Hpyloriin gastric carcinogenesis. METHODS： Hpyloriwas assessed by rapid urease test and Warthin-Starry method, and expression of Bax protein was examined immunohistochemically in 72 patients with pre-malignant lesions. RESULTS： Bax protein was differently expressed in intestinal metaplasia and gastric dysplasia, and showed 63.99% positivity. The positivity of Bax protein expression in Hpylori-positive gastric precancerous lesions （72.3%） was significantly higher than that in H pylori-negative gastric precancerous lesions （48.0%, x^2= 4.191, P〈0.05）. Hpyloriinfection was well correlated with the expression of Bax protein in gastric precancerous lesions （r= 0.978, P〈0.01）. After eradication of H pylori, the positivity of Bax protein expression significantly decreased in Hpylori-positive gastric precancerous lesions （x^2 = 5.506, P〈0.05）. In the persisting H pylori-infected patients, the positivity of Bax protein expression was not changed. CONCLUSION： H pyloriinfection may be involved in the upregulation of Bax gene, which might be one of the mechanisms of Hpyloriinfection-induced gastric epithelial cell apoptosis. Hpylorimight act as a tumor promoter in the genesis of gastric carcinoma and eradication of Hpylori could inhibit gastric carcinogenesis.