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Gastroduodenal mucosal defense.

机译:胃十二指肠粘膜防御。

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摘要

PURPOSE OF REVIEW: The gastroduodenum has multiple means by which it resists injury from intrinsic and extrinsic factors, including gastric acid, nonsteroidal anti-inflammatory drugs, and Helicobacter pylori. We review recent insights into the mechanisms by which the gastroduodenum resists injury and discuss factors contributing to defensive failure. RECENT FINDINGS: Duodenal bicarbonate secretion, a primary defensive mechanism, is mediated by the downregulated in adenoma anion exchanger and is stimulated by estrogens. Nonsteroidal anti-inflammatory drug gastric damage is dependent on toll-like receptor signaling. Portal hypertensive gastropathy impairs extracellular signal-regulated kinase 1/2 phosphorylation, increasing oxidative stress. H. pylori-induced peptic ulcer disease is associated with inadequate regulatory T cell responses. SUMMARY: Enhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight into potential therapeutic targets, which contributes towards the development of more well tolerated and more effective therapies.
机译:审查目的:十二指肠具有多种抵抗内在和外在因素(包括胃酸,非甾体类抗炎药和幽门螺杆菌)的方法。我们回顾了胃十二指肠抵抗损伤的机制的最新见解,并讨论了导致防御失败的因素。最近的发现:十二指肠碳酸氢盐的分泌是一种主要的防御机制,是由腺瘤阴离子交换剂的下调介导的,并受到雌激素的刺激。非甾体抗炎药的胃损害取决于toll样受体信号转导。门脉高压性胃病损害细胞外信号调节激酶1/2磷酸化,增加氧化应激。幽门螺杆菌诱发的消化性溃疡疾病与调节性T细胞反应不足有关。摘要:对胃十二指肠防御和损伤机制的加深了解为潜在的治疗靶标提供了新的见识,这有助于开发更好的耐受性和更有效的疗法。

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