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  • Title: [Chronic Helicobacter pylori infection induces the proliferation and apoptosis in gastric epithelial cells and gastric precancerosis in Mongolian gerbils].
    Author: Wang F, Pan J, Luo L, Huang L, Lu H, Guo Q, Xu C, Shen S.
    Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2011 Sep; 36(9):865-71. PubMed ID: 21946211.
    Abstract:
    OBJECTIVE: To explore the effect of different Helicobacter pylori (H.pylori) clinical strains on the proliferation and apoptosis of gastric epithelial cells, and to observe the effect of H.pylori on gastric mucosa by Mongolian gerbil model infected H.pylori. METHODS: H.pylori isolates harvested from pathologically documented gastric carcinoma (GC, n=10) or chronic gastritis specimens (CG, n=10) were co-cultured with GES-1 cells individually. MTT assay and flow cytometry were used to determine the proliferation and apoptosis of GES-1 cells induced by H.pylori isolates. Mongolian gerbils were infected by the most (A strain) and the least (B strain) significantly proliferated H.pylori strains. Results When co-cultured with the cell/bacteria concentration ratio 1:1 and 1:50 for 12 h and the cell/bacteria concentration ratio 1:50 for 24 h, H.pylori clinical strains isolated from patients with gastric cancer promoted the proliferation of GES-1 cells, and there was significant difference in the absorbance compared with the group of gastritis strains(P<0.05). The apoptosis rate of the GC and CG groups increased significantly (P<0.05) compared with the control group when co-cultured with the cell/bacteria concentration ratio 1:50 and 1:200, and there was no significant difference between the GC group and the CG group (P>0.05). The incidences of intestinal metaplasia and dysplasia in the A strain group were significantly higher than those in the B strain group (P<0.05). CONCLUSION: H.pylori strains from different disease sources have different effects on the proliferation of GES-1 cells. H.pylori isolated from gastric cancer can promote the proliferation of cells to different degrees and directly induce gastric precancerosis and gastric cancer.
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