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目的分析CagA+幽门螺杆菌及不同激酶抑制剂对幽门螺杆菌诱导人正常胃粘膜上皮细胞白细胞介素-1β(IL-1β)分泌的影响。方法 将CagA+幽门螺杆菌与人正常胃粘膜上皮细胞系(GES-1)细胞共同培养,IL-1β分泌用酶联免疫吸附试验进行检测,比较蛋白激素A、C、G和蛋白酪氨酸激酶的抑制剂对幽门螺杆菌诱导胃上皮细胞IL-1β分泌的影响。结果 CagA+幽门螺杆菌显著增加胃上皮细胞IL-1β的分泌;蛋白激酶A、C、G的抑制剂不能阴断幽门螺杆菌诱导的GES-1分泌IL-1β,而蛋白酪氨酸激酶的抑制剂可阻断这种IL-1β的分泌。结论 CagA+基因型幽门螺杆菌可显著增加胃粘膜上皮细胞IL-1β的分泌并且依赖于蛋白酪氨酸激酶的活性。
Objective To analyze the influence of CagA + Helicobacter pylori and different kinase inhibitors on the secretion of interleukin-1β (IL-1β) induced by Helicobacter pylori in human normal gastric epithelial cells. Methods CagA + Helicobacter pylori was co-cultured with human normal gastric mucosa epithelial cell line (GES-1) cells. The secretion of IL-1β was detected by enzyme-linked immunosorbent assay. The levels of protein hormone A, C, G and protein tyrosine kinase On Helicobacter pylori-induced secretion of IL-1β in gastric epithelial cells. Results CagA + Helicobacter pylori significantly increased the secretion of IL-1β in gastric epithelial cells. Inhibitors of protein kinases A, C and G did not inactivate H. pylori-induced secretion of IL-1β by GES-1, while inhibition of protein tyrosine kinase Agents can block the secretion of this IL-1β. Conclusion CagA + genotype Helicobacter pylori can significantly increase the secretion of IL-1β in gastric epithelial cells and depend on the activity of protein tyrosine kinase.