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J Biomed Sci ; 21: 96, 2014 Oct 09.
Artículo en Inglés | MEDLINE | ID: mdl-25296847

RESUMEN

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.We used two strains to investigate whether H. pylori growth, viability, adhesion and CagA-phosphorylation 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 dose-dependent. 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.


Asunto(s)
Adhesión Bacteriana/efectos de los fármacos , Sistemas de Secreción Bacterianos/efectos de los fármacos , Glucosa/farmacología , Helicobacter pylori/metabolismo , Helicobacter pylori/patogenicidad , Edulcorantes/farmacología , Antígenos Bacterianos/metabolismo , Proteínas Bacterianas/metabolismo , Línea Celular Tumoral , Infecciones por Helicobacter/metabolismo , Infecciones por Helicobacter/patología , Humanos , Fosforilación/efectos de los fármacos
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