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胃十二指肠黏膜防御。

Gastroduodenal mucosal defense.

机构信息

aCedars-Sinai Medical Residency Program bGreater Los Angeles Veteran Affairs Healthcare System, WLAVA Medical Center cDepartment of Medicine dDepartment of Surgery, UCLA School of Medicine eCURE: Digestive Diseases Research Center Department of Medicine fBrentwood Biomedical Research Institute, Los Angeles, California, USA.

出版信息

Curr Opin Gastroenterol. 2013 Nov;29(6):642-9. doi: 10.1097/MOG.0b013e328365d42e.

DOI:10.1097/MOG.0b013e328365d42e
PMID:24100725
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7193727/
Abstract

PURPOSE OF REVIEW

To review recent developments in the field of gastroduodenal mucosal defense.

RECENT FINDINGS

Research in the field of gastroduodenal mucosal defense has focused on continued elucidation of molecular mechanisms that protect the mucosa and influence healing at the cellular level. Review of literature over the past year reveals focus on familiar processes such as superoxide dismutase, nitric oxide, heme oxygenase-1, neutrophil infiltration, cysteamine, mucin, hydrogen sulfide, ghrelin, adiponectin and the influence of Helicobacter pylori, but also brings into light new processes such as the balance between apoptosis and cellular proliferation, as well as the influence of other organ systems such as the bone marrow and central nervous system on the gastrointestinal tract.

SUMMARY

These new published findings contribute to our overall understanding of gastroduodenal defense and suggest innovative avenues of future research and possible novel therapeutic targets.

摘要

目的综述

综述胃十二指肠黏膜防御领域的最新进展。

最新发现

胃十二指肠黏膜防御领域的研究集中于阐明保护黏膜和影响细胞水平愈合的分子机制。对过去一年文献的回顾表明,研究重点是熟悉的过程,如超氧化物歧化酶、一氧化氮、血红素加氧酶-1、中性粒细胞浸润、半胱胺、粘蛋白、硫化氢、胃饥饿素、脂联素以及幽门螺杆菌的影响,但也揭示了新的过程,如细胞凋亡和细胞增殖之间的平衡,以及骨髓和中枢神经系统等其他器官系统对胃肠道的影响。

总结

这些新发表的发现有助于我们全面了解胃十二指肠防御,并为未来的研究和可能的新治疗靶点提供了创新途径。

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Biological activity of Helicobacter pylori components in mammalian cells: is it independent of proteinase-activated receptors?幽门螺杆菌成分在哺乳动物细胞中的生物学活性:是否独立于蛋白酶激活受体?
J Physiol Pharmacol. 2012 Dec;63(6):571-6.
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Metabolic profiling to identify potential serum biomarkers for gastric ulceration induced by nonsteroid anti-inflammatory drugs.代谢组学分析鉴定非甾体类抗炎药致胃黏膜损伤血清生物标志物
J Proteome Res. 2013 Mar 1;12(3):1399-407. doi: 10.1021/pr3010452. Epub 2013 Feb 6.
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Substance P induces gastric mucosal protection at supraspinal level via increasing the level of endomorphin-2 in rats.
膳食硝酸盐与心血管疾病流行病学:美国国立心肺血液研究所研讨会报告
J Am Heart Assoc. 2016 Jul 6;5(7):e003402. doi: 10.1161/JAHA.116.003402.
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Dual Alpha2C/5HT1A Receptor Agonist Allyphenyline Induces Gastroprotection and Inhibits Fundic and Colonic Contractility.双重α2C/5-羟色胺1A受体激动剂烯丙苯心安诱导胃保护并抑制胃底和结肠收缩力。
Dig Dis Sci. 2016 Jun;61(6):1512-23. doi: 10.1007/s10620-015-4026-9. Epub 2016 Feb 10.
P 物质通过增加大鼠中内吗啡肽-2 的水平在上中枢水平诱导胃黏膜保护。
Brain Res Bull. 2013 Feb;91:38-45. doi: 10.1016/j.brainresbull.2013.01.004. Epub 2013 Jan 14.
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Musashi-1 post-transcriptionally enhances phosphotyrosine-binding domain-containing m-Numb protein expression in regenerating gastric mucosa.Musashi-1 在后转录水平增强再生胃黏膜中含磷酸酪氨酸结合域的 m-Numb 蛋白表达。
PLoS One. 2013;8(1):e53540. doi: 10.1371/journal.pone.0053540. Epub 2013 Jan 4.
5
Cytoglobin may be involved in the healing process of gastric mucosal injuries in the late phase without angiogenesis.细胞血红素可能参与了无血管生成的晚期胃黏膜损伤的愈合过程。
Dig Dis Sci. 2013 May;58(5):1198-206. doi: 10.1007/s10620-012-2514-8. Epub 2013 Jan 10.
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Increased oxidative stress may lead to impaired adaptive cytoprotection in the gastric mucosa of portal hypertensive rat.氧化应激增加可能导致门脉高压大鼠胃黏膜适应性细胞保护受损。
J Gastroenterol Hepatol. 2013 Apr;28(4):639-44. doi: 10.1111/jgh.12101.
7
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Free Radic Biol Med. 2013 Apr;57:61-7. doi: 10.1016/j.freeradbiomed.2012.12.015. Epub 2012 Dec 28.
8
Helicobacter pylori infection impairs the mucin production rate and turnover in the murine gastric mucosa.幽门螺杆菌感染会损害小鼠胃黏膜的粘蛋白产生速率和周转率。
Infect Immun. 2013 Mar;81(3):829-37. doi: 10.1128/IAI.01000-12. Epub 2012 Dec 28.
9
Asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, interacts with gastric oxidative metabolism and enhances stress-induced gastric lesions.不对称二甲基精氨酸,一种内源性一氧化氮合酶抑制剂,与胃氧化代谢相互作用,增强应激引起的胃损伤。
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Alpha-lipoic acid protects against indomethacin-induced gastric oxidative toxicity by modulating antioxidant system.硫辛酸通过调节抗氧化系统来防止消炎痛引起的胃氧化毒性。
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