Abstract
BackgroundBoth H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, however, the interaction pattern of the two is not very clear. Our objective was to investigate the effects of NaCl-pretreated H. pylori on DNA damage and proliferation of gastric epithelial cell (GES-1).MethodsGES-1 cells were co-cultured with H.pylori or NaCl-pretreated H. pylori (with 30% NaCl) for 24 h. The morphological changes of all cells were observed by inverted phase contrast microscopy and transmission electron microscopy. Oxidative DNA damage was examined by immunofluorescence. Alterations in mitochondrial membrane potential and apoptosis rate were detected by flow cytometry and western blot, and expression of Ki-67, PCNA and P21 were evaluated using the immunocytochemical staining.ResultsGES-1 cells co-cultured with NaCl-pretreated H.pylori exhibited morphological changes and oxidative DNA damage. Although no significant disruption of the mitochondrial membrane potential (ΔΨm) and apoptotic rate were observed compared with control groups, there were significant decreased in Bax and Caspase3 proteins and increased in Bcl-2 protein in GES-1 cells infected with H. pylori30 when compared with GES-1 cells cultured with H. pylori. In addition, we found a proliferative effect on GES-1 cells with an increased expression of Ki-67 and PCNA as well as a decreased p21 expression, through which the cells may acquire the potential for malignant transformation.ConclusionNaCl-pretreated H. pylori possessed the ability to cause cell injury and promote proliferation in gastric epithelial cells.
Highlights
Both H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, the interaction pattern of the two is not very clear
We found that the expression of 8-OHdG in GES-1 cells cultured with H. pylori30 was significantly decreased when compared with GES-1 cells cultured with H. pylori (Figure 2A-D, P < 0.05)
The results suggested that there were significant increased in Bax and Caspase3 proteins and decreased in Bcl-2 protein in GES-1 cells infected with H. pylori and H. pylori30
Summary
Both H. pylori infection and high salt (NaCl) diet are risks of gastric cancer, the interaction pattern of the two is not very clear. Our objective was to investigate the effects of NaCl-pretreated H. pylori on DNA damage and proliferation of gastric epithelial cell (GES-1). Epidemiological evidence suggested a positive association between high salt or and H. pylori infection in gastric diseases [1]. Some contaminated foods or water, including those with very high NaCl concentrations may serve as reservoirs for the transmission of H.pylori [2]. It is important to investigate the survivability and self-regulation of H.pylori exposed to high salt concentrations. Among the pathogenic mechanisms relevant to gastric carcinogenesis and correlated with H. pylori infection, it has been demonstrated that the production of reactive oxygen species (ROS) and subsequent damage to DNA may be quite important. H. pylori-associated inflammation is indicated by increased levels of oxidative DNA damage, and increased
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