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目的:研究ITF对胃黏膜上皮细胞增殖和迁移的影响,及ERK1/2信号通路在其中的作用。方法:以GES-1细胞为研究对象,用Western blot检测ITF对ERK1/2信号通路的作用,以不同浓度ITF及ERK1/2信号通路抑制剂U0126处理GES-1细胞,用CCK-8检测细胞增殖,用细胞穿孔实验观察细胞迁移。比较不同浓度ITF对GES-1细胞增殖和迁移的影响,及ERK1/2信号通路在其中的作用。结果:ITF提高了pERK1/2蛋白的表达水平,U0126抑制了ITF激活的pERK1/2蛋白的表达。与对照组比较,在细胞培养的24h后,ITF以剂量依赖的方式促进了GES-1细胞的增殖和迁移。U0126抑制了ITF对GES-1细胞的促增殖和迁移作用。结论:肠三叶因子通过激活ERK1/2信号通路促进胃黏膜上皮细胞增殖和迁移。
Objective: To investigate the effect of ITF on the proliferation and migration of gastric mucosal epithelial cells and the role of ERK1 / 2 signal transduction pathway. Methods: The effect of ITF on ERK1 / 2 signal transduction pathway was detected by Western blot. GES-1 cells were treated with different concentrations of ITF and ERK1 / 2 inhibitor U0126, and the cells were detected by CCK-8 Proliferation, cell migration experiments were observed with cell perforation experiments. The effects of different concentrations of ITF on the proliferation and migration of GES-1 cells were compared, and the role of ERK1 / 2 signal transduction pathway was also discussed. Results: ITF increased the expression of pERK1 / 2 protein and U0126 inhibited the expression of ITF-activated pERK1 / 2 protein. Compared with the control group, ITF promoted the proliferation and migration of GES-1 cells in a dose-dependent manner after 24h of cell culture. U0126 inhibits ITF on the proliferation and migration of GES-1 cells. Conclusion: Gut trefoil factor can promote the proliferation and migration of gastric mucosal epithelial cells by activating ERK1 / 2 signaling pathway.