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Deoxycholic Acid Could Induce Apoptosis and Trigger Gastric Carcinogenesis on Gastric Epithelial Cells by Quantitative Proteomic Analysis

机译:通过定量蛋白质组学分析脱氧胆酸可以诱导胃上皮细胞凋亡并触发胃癌发生。

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摘要

Background. Pathologic duodenogastric reflux can induce or aggravate gastritis because of the presence of bile acids. Bile reflux has been generally considered to be associated with intestinal metaplasia and gastric cancer. However, the pathogenic mechanisms of the effects of bile acids on gastric mucosa are still unknown. Methods. To explore the mechanisms by which bile acids induce gastric mucosal lesions, we examined cell apoptosis in the gastric epithelial cell line GES-1 and investigated the changes in protein profiles of GES-1 cells in response to a bile acid deoxycholic acid using a proteomics approach. Changes in the profiles of the differently expressed proteins were analyzed using the DAVID and STRING programs. Results. We found apoptosis was significantly induced in GES-1 cells by deoxycholic acid. Using liquid chromatographic/tandem mass spectrometric (LC-MS/MS) methods, 134 upregulated proteins and 214 downregulated proteins were identified in the bile acid treated GES-1 cells. Bioinformatics analysis revealed the interactions and signaling networks of these differentially expressed proteins. Conclusion. These findings may improve the understanding of the molecular mechanisms underlying the pathogenicity of bile acids on gastric mucosa.
机译:背景。由于胆汁酸的存在,病理性十二指肠胃返流会诱发或加重胃炎。胆汁反流通常被认为与肠上皮化生和胃癌有关。然而,胆汁酸对胃粘膜的致病机制仍不清楚。方法。为了探索胆汁酸诱导胃粘膜损伤的机制,我们使用蛋白质组学方法检查了胃上皮细胞系GES-1中的细胞凋亡,并研究了GES-1细胞响应胆汁酸脱氧胆酸的蛋白谱变化。 。使用DAVID和STRING程序分析了不同表达的蛋白质的概况变化。结果。我们发现脱氧胆酸可显着诱导GES-1细胞凋亡。使用液相色谱/串联质谱(LC-MS / MS)方法,在胆汁酸处理过的GES-1细胞中鉴定出134个上调蛋白和214个下调蛋白。生物信息学分析揭示了这些差异表达蛋白的相互作用和信号网络。结论。这些发现可以增进对胆汁酸在胃粘膜上致病性的分子机制的理解。

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