Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016:2016:6720575.
doi: 10.1155/2016/6720575. Epub 2016 Jul 14.

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

Chao Yu  1 , Zhen Wang  1 , Shanjun Tan  2 , Qiang Wang  1 , Chunyu Zhou  1 , Xin Kang  1 , Shuang Zhao  1 , Shuai Liu  1 , Huijun Fu  3 , Zhen Yu  4 , Ai Peng  1
Affiliations

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

Chao Yu et al. Gastroenterol Res Pract. 2016.

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Serum levels of blood urea nitrogen and creatinine in each group in postoperative week 4. Data are expressed as mean ± SD. ∗ P < 0.05, versus control group.
Figure 2
Figure 2
Serum levels of inflammatory cytokines TNF-α, IL-6, and IL-10 in each group. POW: postoperative week. Data are expressed as mean ± SD. ∗ P < 0.05, versus control group at the same time point.
Figure 3
Figure 3
Serum LA levels and DAO activity in each group. POW: postoperative week. Data are expressed as mean ± SD. ∗ P < 0.05, versus control group at the same time point.
Figure 4
Figure 4
Intestinal clearance of FD4 in each group. POW: postoperative week. Data are expressed as mean ± SD. ∗ P < 0.05, versus control group at the same time point.
Figure 5
Figure 5
Representative microscopic changes of the intestinal tissue stained with H&E using light microscopy (100x) in each group. POW: postoperative week. There were time-dependent edema and inflammation in the intestinal mucosa and submucosa in uremia group when compared with those in the control group, especially in postoperative weeks 8 and 10.
Figure 6
Figure 6
Chiu's score in each group. ND: not detectable; POW: postoperative week. Data are expressed as the mean ± SD. ∗ P < 0.05, versus uremia group in POW 4.
Figure 7
Figure 7
The intestinal levels of MDA, SOD, CAT, and GSH-PX in each group. POW: postoperative week. Data are expressed as mean ± SD. ∗ P < 0.05, versus control group at the same time point.
See this image and copyright information in PMC

References

    1. Jiang Z., Zhang X., Yang L., Li Z., Qin W. Effect of restricted protein diet supplemented with keto analogues in chronic kidney disease: a systematic review and meta-analysis. International Urology and Nephrology. 2016;48(3):409–418. doi: 10.1007/s11255-015-1170-2. - DOI - PubMed
    1. Breidthardt T., Moser-Bucher C. N., Praehauser C., et al. Morbidity and mortality on chronic haemodialysis: a 10-year Swiss single centre analysis. Swiss Medical Weekly. 2011;141 doi: 10.4414/smw.2011.13150.w13150 - DOI - PubMed
    1. Lozano R., Naghavi M., Foreman K., et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. The Lancet. 2012;380(9859):2095–2128. - PMC - PubMed
    1. Rebollo-Rubio A., Morales-Asencio J. M., Pons-Raventos M. E., Mansilla-Francisco J. J. Review of studies on health related quality of life in patients with advanced chronic kidney disease in Spain. Nefrologia. 2015;35(1):92–109. doi: 10.3265/Nefrologia.pre2014.Jul.12133. - DOI - PubMed
    1. Hedgeman E., Lipworth L., Lowe K., Saran R., Do T., Fryzek J. International burden of chronic kidney disease and secondary hyperparathyroidism: a systematic review of the literature and available data. International Journal of Nephrology. 2015;2015:15. doi: 10.1155/2015/184321.184321 - DOI - PMC - PubMed

LinkOut - more resources