Gastroduodenal mucosal defense
Gastroduodenal mucosal defense
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DOI：
10.1097/mog.0b013e32833f1222
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发表时间：
2010-11-01
影响因子：
2.5
通讯作者：
Kaunitz, Jonathan D.
中科院分区：
文献类型：
--
作者：
deFoneska, Arushi;Kaunitz, Jonathan D.
回顾的目的我们总结了最近的研究结果有关胃十二指肠粘膜防御以及防御失败的因素，突出的结果，阐明新的病理生理mechanism.Recent findingsGastroduodenal碳酸氢盐分泌介导的前列腺素E受体和前列腺素lubiprostone刺激。Toll样受体（TLR）4信号转导对胃损伤具有保护作用。肠碱性磷酸酶（IAP）是一种化学传感器，调节十二指肠粘膜表面pH值。脂多糖（LPS）增加胃的通透性，脂肪消化过程中分泌的IAP可以解毒结肠LPS。NADPH氧化酶活性介导缺血/再灌注相关胃粘膜损伤热休克蛋白70（HSP 70）通过抑制细胞凋亡、促炎细胞因子和细胞粘附分子（CAM）来保护胃粘膜。HSP 90可能是适应性细胞保护受损的一个因素。蛋白酶激活受体-1（PAR-1）通过抑制促炎途径介导对幽门螺杆菌诱导的胃炎具有保护作用。IKK β/NF-κ B信号通过抑制细胞凋亡和坏死减少慢性螺杆菌诱导的炎症A（2A）腺苷受体的激活减少炎症和胃炎，但导致持续的幽门螺杆菌infection.SummaryEnhanced胃十二指肠防御和损伤的机制的理解提供了新的见解潜在的治疗靶点，有助于更好的耐受性和更有效的治疗方法的发展。
Purpose of reviewWe have summarized recent findings related to gastroduodenal mucosal defense as well as factors contributing to defensive failure, highlighting findings that illuminate new pathophysiological mechanisms.Recent findingsGastroduodenal bicarbonate secretion is mediated by prostaglandin E receptors and stimulated by the prostone lubiprostone. Toll-like receptor (TLR)4 signaling is protective against gastric injury. Intestinal alkaline phosphatase (IAP) is a chemosensor that regulates the duodenal mucosal surface pH. Lipopolysaccharide (LPS) increases gastric permeability; IAP secreted during fat digestion may detoxify colonic LPS. NADPH oxidase activity mediates ischemia/reperfusion-related gastric mucosal damage. Heat shock protein 70 (HSP70) protects the gastric mucosa through inhibition of apoptosis, proinflammatory cytokines, and cell adhesion molecules (CAMs). HSP90 may be a contributing factor in impaired adaptive cytoprotection. Proteinase-activated receptor-1 (PAR-1) is protective against Helicobacter-induced gastritis, mediated by the suppression of proinflammatory pathways. IKK beta/NF-kappa B signaling decreases chronic Helicobacter-induced inflammation by inhibiting cellular apoptosis and necrosis. Activation of A(2A) adenosine receptors decreases inflammation and gastritis but leads to persistent Helicobacter pylori infection.SummaryEnhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight into potential therapeutic targets, contributing towards the development of better tolerated and more effective therapies.