- 作者: Shew-Meei Sheu, Hsin Cheng, Cheng-Ye Kao, Yao-Jong Yang, Jiunn-Jong Wu ,Bor-Shyang Sheu
- 作者服務機構: Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan R.O.C
- 中文摘要: --
- 英文摘要:
Background:
Hyperglycemia increases the risk of gastric cancer in H. pylori-infected patients. High glucose could increase endothelial permeability and cancer-associated signaling. These suggest high glucose may affect H. pylori or its infected statusWe used two strains to investigate whether H. pylori growth, viability, adhesion and CagAphosphorylation level in the infected-AGS cells were influenced by glucose concentration (100, 150, and 200 mg/dL).
Results:
The growth curves of both strains in 200 mg/dL of glucose were maintained at the highest optimal density after 48 h and the best viability of both strains were retained in the same glucose condition at 72 h. Furthermore, adhesion enhancement of H. pylori was significantly higher in 200 mg/dL of glucose as compared to that in 100 and 150 mg/dL (p < 0.05). CagA protein also increased in higher glucose condition. The cell-associated CagA and
phosphorylated-CagA was significantly increased in 150 and 200 mg/dL of glucose concentrations as compared to that of 100 mg/dL (p < 0.05), which were found to be dosedependent.
Conclusion:
Higher glucose could maintain H. pylori growth and viability after 48 h. H. pylori adhesion and CagA increased to further facilitate the enhancement of cell-associated CagA and phosphorylated CagA in higher glucose conditions. - 中文關鍵字: --
- 英文關鍵字: Background Hyperglycemia increases the risk of gastric cancer in H. pylori-infected patients. High glucose could increase endothelial permeability and cancer-associated signaling. These suggest high glucose may affect H. pylori or its infected status.