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本文引用的文献

1
Targeting the transcription factor Nrf2 to ameliorate oxidative stress and inflammation in chronic kidney disease.针对转录因子 Nrf2 改善慢性肾脏病中的氧化应激和炎症。
Kidney Int. 2013 Jun;83(6):1029-41. doi: 10.1038/ki.2012.439. Epub 2013 Jan 16.
2
Disintegration of colonic epithelial tight junction in uremia: a likely cause of CKD-associated inflammation.尿毒症中结肠上皮紧密连接的解体:CKD 相关炎症的一个可能原因。
Nephrol Dial Transplant. 2012 Jul;27(7):2686-93. doi: 10.1093/ndt/gfr624. Epub 2011 Nov 29.
3
Colonic contribution to uremic solutes.肠道对尿毒症溶质的贡献。
J Am Soc Nephrol. 2011 Sep;22(9):1769-76. doi: 10.1681/ASN.2010121220. Epub 2011 Jul 22.
4
Intestinal-renal syndrome: mirage or reality?肠-肾综合征:海市蜃楼还是现实?
Blood Purif. 2011;31(1-3):70-6. doi: 10.1159/000321848. Epub 2011 Jan 10.
5
Contribution of impaired Nrf2-Keap1 pathway to oxidative stress and inflammation in chronic renal failure.慢性肾衰竭中 Nrf2-Keap1 通路功能障碍对氧化应激和炎症的贡献。
Am J Physiol Renal Physiol. 2010 Mar;298(3):F662-71. doi: 10.1152/ajprenal.00421.2009. Epub 2009 Dec 9.
6
Intestinal mucosal barrier function in health and disease.健康与疾病状态下的肠道黏膜屏障功能
Nat Rev Immunol. 2009 Nov;9(11):799-809. doi: 10.1038/nri2653.
7
Soluble CD14 levels, interleukin 6, and mortality among prevalent hemodialysis patients.维持性血液透析患者的可溶性CD14水平、白细胞介素6与死亡率
Am J Kidney Dis. 2009 Dec;54(6):1072-80. doi: 10.1053/j.ajkd.2009.06.022. Epub 2009 Sep 6.
8
Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease.氧化应激与炎症:慢性肾脏病和心血管疾病之间的联系
Kidney Int Suppl. 2008 Dec(111):S4-9. doi: 10.1038/ki.2008.516.
9
Modulation of the maturing gut barrier and microbiota: a novel target in allergic disease.成熟肠道屏障与微生物群的调节:过敏性疾病的新靶点。
Curr Pharm Des. 2008;14(14):1368-75. doi: 10.2174/138161208784480207.
10
Endotoxemia is related to systemic inflammation and atherosclerosis in peritoneal dialysis patients.内毒素血症与腹膜透析患者的全身炎症及动脉粥样硬化有关。
Clin J Am Soc Nephrol. 2008 Mar;3(2):431-6. doi: 10.2215/CJN.03600807. Epub 2008 Feb 6.

慢性肾脏病会损害肠道的屏障功能并改变其微生物菌群:这是导致炎症和尿毒症毒性的主要环节。

CKD impairs barrier function and alters microbial flora of the intestine: a major link to inflammation and uremic toxicity.

机构信息

Division of Nephrology and Hypertension, Departments of Medicine and Physiology & Biophysics, University of California, Irvine, California 92868, USA.

出版信息

Curr Opin Nephrol Hypertens. 2012 Nov;21(6):587-92. doi: 10.1097/MNH.0b013e328358c8d5.

DOI:10.1097/MNH.0b013e328358c8d5
PMID:23010760
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3756830/
Abstract

PURPOSE OF REVIEW

Chronic kidney disease (CKD) is associated with oxidative stress and inflammation which contribute to progression of kidney disease and its numerous complications. Until recently, little attention had been paid to the role of the intestine and its microbial flora in the pathogenesis of CKD-associated inflammation. This article is intended to provide an over view of the impact of uremia on the structure and function of the gut and its microbial flora and their potential link to the associated systemic inflammation.

RECENT FINDINGS

Recent studies conducted in the author's laboratories have demonstrated marked disintegration of the colonic epithelial barrier structure and significant alteration of the colonic bacterial flora in humans and animals with advanced CKD. The observed disruption of the intestinal epithelial barrier complex can play an important part in the development of systemic inflammation by enabling influx of endotoxin and other noxious luminal contents into the systemic circulation. Similarly via disruption of the normal symbiotic relationship and production, absorption and retention of noxious products, alteration of the microbial flora can contribute to systemic inflammation and uremic toxicity. In fact recent studies have documented the role of colonic bacteria as the primary source of several well known pro-inflammatory/pro-oxidant uremic toxins as well as many as-yet unidentified retained compounds.

SUMMARY

CKD results in disruption of the intestinal barrier structure and marked alteration of its microbial flora - events that play a major role in the pathogenesis of inflammation and uremic toxicity.

摘要

目的综述

慢性肾脏病(CKD)与氧化应激和炎症有关,这些因素导致肾脏疾病及其许多并发症的进展。直到最近,人们对肠道及其微生物菌群在 CKD 相关炎症发病机制中的作用还关注甚少。本文旨在概述尿毒症对肠道结构和功能及其微生物菌群的影响,以及它们与相关系统性炎症的潜在联系。

最新发现

作者实验室最近进行的研究表明,在晚期 CKD 患者中,肠道上皮屏障结构明显解体,肠道细菌菌群发生重大改变。观察到的肠道上皮屏障复合体的破坏可能通过使内毒素和其他有害腔内容物进入全身循环,在系统性炎症的发展中发挥重要作用。同样,通过破坏正常的共生关系以及有害物质的产生、吸收和保留,微生物菌群的改变也可能导致系统性炎症和尿毒症毒性。事实上,最近的研究已经证明了结肠细菌作为几种众所周知的促炎/促氧化剂尿毒症毒素以及许多尚未确定的保留化合物的主要来源的作用。

总结

CKD 导致肠道屏障结构破坏和微生物菌群明显改变,这些事件在炎症和尿毒症毒性的发病机制中起主要作用。