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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)
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Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2)

机译:肠三叶因子(ITF)通过激活细胞外信号调节激酶1/2(ERK1 / 2)对胃粘膜上皮的保护作用

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摘要

The rapid repair of gastric mucosa is critical upon exposure to injurious agents. Intestinal trefoil factor (ITF) is a member of the trefoil factor family domain peptides, which play an important role in the cytoprotection of gastric epithelium. However, the underlying molecular mechanisms that are responsible for ITF-induced gastric epithelial repair remain unclear. In the present study, we demonstrate that ITF enhances the proliferation and migration of GES-1 gastric endothelial cells in a doseand time-dependent manner through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the ITF-mediated protection of GES-1 cells from a NS398 (nonsteroidal anti-inflammatory drug) was dependent on the ERK1/2 signaling pathway. Taken together, the results provide a mechanistic explanation for ITF-mediated protection of gastric epithelial mucosa cells, suggesting that activation of the ERK1/2 signaling pathway may provide a new therapeutic strategy for repairing gastric injury.
机译:暴露于有害物质后,胃粘膜的快速修复至关重要。肠三叶因子(ITF)是三叶因子家族域肽的成​​员,在胃上皮细胞的细胞保护中起重要作用。但是,负责ITF诱导的胃上皮修复的基本分子机制仍不清楚。在本研究中,我们证明ITF通过激活细胞外信号调节激酶1/2(ERK1 / 2),以剂量和时间依赖的方式增强GES-1胃内皮细胞的增殖和迁移。此外,ITF介导的GES-1细胞免受NS398(非甾体类抗炎药)的保护依赖于ERK1 / 2信号通路。综上所述,这些结果为ITF介导的胃上皮黏膜细胞保护提供了机械学解释,表明ERK1 / 2信号通路的激活可能提供修复胃损伤的新治疗策略。

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