瞄准:探索 H pylori 由引起胃的上皮细胞的激活的机制。方法:VacA (+) 和 CagA (+) 标准 H pylori 线 NCTC 11637 和人的胃的腺癌导出胃的上皮的房间线 BGC-823 在学习被使用。MTT 试金并且(3 ) H-TdR 加入测试被用来检测 BGC-823 房间的增长,西方的弄污被用来检测相关蛋白质的活动和存在。结果:有 H pylori 摘录的孵化增加了胃的上皮细胞的增长,现场由两个思考了房间数字和 DNA 合成率。细胞外的调整信号的蛋白质激酶(英皇家空军之阶级最低之兵) 的活动表明与 H pylori 摘录在孵化以后在 20 min 以内增加并且看起来是一个持续事件的转导变异串联。MAPK/ERK 激酶(MEK ) 禁止者 PD98059 在两项英皇家空军之阶级最低之兵活动和房间增长废除了 H pylori 摘录的行动。有 H pylori 的孵化提取增加的 c-Fos 表示和 SRE 依赖的基因表示。与 97.4 kDa 和酷氨酸激酶禁止者 genistein 的分子的尺寸包括蛋白质引起几蛋白质的磷酸化的 H pylori 摘录禁止了英皇家空军之阶级最低之兵的激活和 H pylori 摘录引起的房间的增长。结论:在 H pylori 的生物学上活跃的元素通过激活酷氨酸激酶提取胃的上皮细胞的原因增长,英皇家空军之阶级最低之兵表明转导变异串联。
AIM: To explore the mechanism by which H pylori causes activation of gastric epithelial cells. METHODS: A VacA (+) and CagA (+) standard Hpylori line NCTC 11637 and a human gastric adenocarcinoma derived gastric epithelial cell line BGC-823 were applied in the study. MTT assay and ^3H-TdR incorporation test were used to detect the proliferation of BGC-823 cells and Western blotting was used to detect the activity and existence of related proteins. RESULTS: Incubation with Hpylori extract increased the proliferation of gastric epithelial cells, reflected by both live cell number and DNA synthesis rate. The activity of extracellular signal-regulated protein kinase (ERK) signal transduction cascade increased within 20 min after incubation with Hpylori extract and appeared to be a sustained event. MAPK/ERK kinase (MEK) inhibitor PD98059 abolished the action of H pylori extract on both ERK activity and cell proliferation. Incubation with H pylori extract increased c-Fos expression and SRE-dependent gene expression. Hpylori extract caused phosphorylation of several proteins including a protein with molecular size of 97.4 kDa and tyrosine kinase inhibitor genistein inhibited the activation of ERK and the proliferation of cells caused by Hpylori extract. CONCLUSION: Biologically active elements in H pylori extract cause proliferation of gastric epithelial cells through activating tyrosine kinase and ERK signal transduction cascade.