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肠道微生态在华支睾吸虫致宿主肝功能损伤中的作用研究
引用本文:蔡连顺,祝丽玲,宫梓琳,张艺莹,孙婷婷,王树清,车世伟.肠道微生态在华支睾吸虫致宿主肝功能损伤中的作用研究[J].中国微生态学杂志,2017(1).
作者姓名:蔡连顺  祝丽玲  宫梓琳  张艺莹  孙婷婷  王树清  车世伟
作者单位:佳木斯大学,佳木斯大学,佳木斯大学,佳木斯大学,秦皇岛市海港医院,佳木斯市中心医院,佳木斯大学
摘    要:目的研究肠道微生态在华支睾吸虫致肝损伤中的作用。方法建立华支睾吸虫感染大鼠模型。分别在造模后48 h、18 d和35 d检测血浆内毒素、ALT(谷丙转氨酶)、AST(谷草转氨酶)水平;检测肠黏液中sIgA含量;取肠内容物进行乳酸杆菌、双歧杆菌、肠球菌和肠杆菌的培养及定量分析。结果造模后18 d、35 d,大鼠血浆内毒素、ALT、AST水平明显升高,差异有统计学意义(t_内=8.335、7.612,t_(ALT)=11.815、9.874,t_(AST)=7.433、8.015,P值均0.01);造模后48 h,肠黏液sIgA水平高于正常组(t=2.752,P0.05),尤以造模后18 d、35 d升高显著(t=13.118、9.546,P值均0.01);造模后48 h、18 d和35 d,肠道乳酸杆菌和双歧杆菌数量明显减少(t_乳=2.612、4.142、5.556,t_(双)=2.302、4.565、3.982,P值0.05或P值0.01),造模后18 d和35 d,肠杆菌和肠球菌数量明显增多(t_肠=4.562、5.247,t肠=5.366、4.775,P值均0.01)。结论华支睾吸虫感染可致大鼠肠道菌群发生失调,引发内毒素血症,参与介导对肝细胞的损伤。

关 键 词:肠道菌群  华支睾吸虫  大鼠  肝功能

The role of gut microflora in the host liver function damage caused by Clonorchis sinensis
Abstract:Abstract: Objective To study the role of intestinal microflora in the host liver damage induced by Clonorchis sinensis. Methods The rat models of Clonorchis sinensis infection were established. The levels of plasma endotoxin, ALT and AST were detected at 48 hours, 18 days and 35 days after modeling. The contents of sIgA in the intestinal mucus were detected. The intestinal contents were cultured for separating Lactobacilli, Bifidobacteria, Enterococci and Enterobacter, and quantitative analysis were conducted. Results The levels of plasma endotoxin, ALT and AST increased obviously 18 days and 35 days after modeling, with significant difference (P<0.01). The contents of sIgA in the intestinal mucous were higher than that of the normal group (P<0.05) at 48 hours after modeling, and increased significantly 18 days and 35 days after modeling (P<0.01). At 48 hours, 18 days and 35 days after modeling, the quantities of intestinal Lactobacilli and Bifidobacteria decreased obviously, while the quantities of Enterococci and Enterococci increased significantly (Ps<0.01). Conclusion Clonorchis sinensis infection can lead to intestinal flora imbalance in rats, cause endotoxemia, and participate in mediating the damage of liver cells.
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