Intestinal microflora in rats with ischemia/reperfusion liver injury

被引:60
作者
Xing H.-C. [1 ]
Li L.-J. [1 ]
Xu K.-J. [1 ]
Shen T. [1 ]
Chen Y.-B. [1 ]
Sheng J.-F. [1 ]
Yu Y.-S. [1 ]
Chen Y.-G. [1 ]
机构
[1] Key Laboratory of Infectious Diseases, Ministry of Public Health of China, Institute of Infectious Diseases, Department of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou
关键词
Bacterial translocation; Endotoxin; Ischemia/reperfusion (I/R); Liver injury; Microflora; R51;
D O I
10.1631/jzus.2005.B0014
中图分类号
学科分类号
摘要
Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. Results: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in the I/R group campared to those in the sham group. Intestinal Bifidobacteria andLactobacilli decreased and intestinal Enterobacterium and Enterococcus, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group. Conclusion: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, which contributes to endotoxemia and bacterial translocation to kidney. © 2005, Zhejiang University Press.
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页码:14 / 21
页数:7
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