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慢性肾脏病所致肠黏膜屏障损伤与肠道氧化应激损伤相关

Chronic Kidney Disease Induced Intestinal Mucosal Barrier Damage Associated with Intestinal Oxidative Stress Injury.

作者信息

Yu Chao, Wang Zhen, Tan Shanjun, Wang Qiang, Zhou Chunyu, Kang Xin, Zhao Shuang, Liu Shuai, Fu Huijun, Yu Zhen, Peng Ai

机构信息

Department of Nephrology & Rheumatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China.

Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

出版信息

Gastroenterol Res Pract. 2016;2016:6720575. doi: 10.1155/2016/6720575. Epub 2016 Jul 14.

Abstract

Background. To investigate whether intestinal mucosal barrier was damaged or not in chronic kidney disease progression and the status of oxidative stress. Methods. Rats were randomized into two groups: a control group and a uremia group. The uremia rat model was induced by 5/6 kidney resection. In postoperative weeks (POW) 4, 6, 8, and 10, eight rats were randomly selected from each group to prepare samples for assessing systemic inflammation, intestinal mucosal barrier changes, and the status of intestinal oxidative stress. Results. The uremia group presented an increase trend over time in the serum tumor necrosis factor-alpha, interleukin-6 (IL-6) and IL-10, serum D-lactate and diamine oxidase, and intestinal permeability, and these biomarkers were significantly higher than those in control group in POW 8 and/or 10. Chiu's scores in uremia group were also increased over time, especially in POW 8 and 10. Furthermore, the intestinal malondialdehyde, superoxide dismutase, and glutathione peroxidase levels were significantly higher in uremia group when compared with those in control group in POW 8 and/or 10. Conclusions. The advanced chronic kidney disease could induce intestinal mucosal barrier damage and further lead to systemic inflammation. The underlying mechanism may be associated with the intestinal oxidative stress injury.

摘要

背景。探讨慢性肾脏病进展过程中肠黏膜屏障是否受损以及氧化应激状态。方法。将大鼠随机分为两组:对照组和尿毒症组。采用5/6肾切除法诱导建立尿毒症大鼠模型。在术后第4、6、8和10周,从每组中随机选取8只大鼠制备样本,以评估全身炎症、肠黏膜屏障变化及肠道氧化应激状态。结果。尿毒症组血清肿瘤坏死因子-α、白细胞介素-6(IL-6)和IL-10、血清D-乳酸和二胺氧化酶以及肠道通透性随时间呈上升趋势,且在术后第8周和/或第10周,这些生物标志物显著高于对照组。尿毒症组的Chiu评分也随时间增加,尤其是在术后第8周和第10周。此外,在术后第8周和/或第10周,尿毒症组肠道丙二醛、超氧化物歧化酶和谷胱甘肽过氧化物酶水平显著高于对照组。结论。晚期慢性肾脏病可导致肠黏膜屏障损伤并进一步引发全身炎症。其潜在机制可能与肠道氧化应激损伤有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dba0/4963601/a21136694fec/GRP2016-6720575.001.jpg

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