[1]黄朝晖,吴雄飞,赵洪雯,等.ApoE-/-小鼠肾动脉狭窄及肾损害特点观察[J].第三军医大学学报,2007,29(19):1844-1847.
 HUANG Zhao-hui,WU Xiong-fei,ZHAO Hong-wen,et al.Atherosclerotic renal artery stenosis and renal injury in apolipoprotein E knockout mouse[J].J Third Mil Med Univ,2007,29(19):1844-1847.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第19期
页码:
1844-1847
栏目:
论著
出版日期:
2007-10-15

文章信息/Info

Title:
Atherosclerotic renal artery stenosis and renal injury in apolipoprotein E knockout mouse
作者:
黄朝晖吴雄飞赵洪雯刘宏王汉民
第三军医大学西南医院肾科
Author(s):
HUANG Zhao-hui WU Xiong-fei ZHAO Hong-wen LIU Hong WANG Han-min
Department of Kidneys, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
关键词:
动脉粥样硬化肾动脉狭窄肾脏病理ApoE-/-小鼠
Keywords:
Patherosclerotic stenosis renal artery stenosis renal pathology apolipoprotein E Knockout mice
分类号:
R322.61; R543.5; R692.160.2
文献标志码:
A
摘要:
目的  建立动脉粥样硬化性肾动脉狭窄(atherosclerotic renal artery stenosis, ARAS)小鼠动物模型,并观察其肾损害特点。  方法  取载脂蛋白E基因缺陷(ApoE-/-)小鼠(25~51周龄)的肾动脉和肾脏,动态观察肾动脉病变进展各阶段相应的肾脏病变。根据ARAS程度分3组(A组:<50%;B组:50%~70%;C组:>70%)。A组又根据斑块是否破裂分为A1(未破裂)和A2(破裂)亚组。  结果  建立了ARAS小鼠动物模型。肾动脉和肾脏的变化是:① A1组未发现其下游肾脏病理改变;②A2组其下游肾内肾小管周围毛细血管减少,肾小管上皮细胞肿胀,电镜下可见细胞内线粒体肿胀;③B组和C组已发生斑块破裂,其肾内肾小管周围毛细血管减少明显,与A2组比较,差异显著(P<0.01);肾小管上皮细胞肿胀、脱落、坏死;肾小管间质病变严重。  结论  ApoE-/-小鼠建立的ARAS模型易行、稳定、重复性好。
Abstract:
Objective    To establish a practical, stable and reliable animal model of atherosclerotic renal artery stenosis (ARAS) in apolipoprotein E knockout (ApoE-/-) mouse and investigate the development of renal injury.      Methods    After the ApoE-/- mouse models aged 25-51 weeks were respectively sacrificed, the renal arteries and the kidneys were obtained. The stenosis degree was measured by elastic fibers straining and analyzed by a software  system. According to the stenosis degree, the renal arteries were divided into 3 groups (A: <50%; B: 50%-70%; C: >70%), and group A was divided into 2 subgroups (A1: stable, A2: unstable) depending on whether the atherosclerotic plaque is ruptured or not.      Results    The mouse model of ARAS was established successfully. Renal pathological changes were not found in group A1. Obvious tubulointerstitial injury was noted in group A2, such as decreased peritubular capillaries (PTC), the broken and disordered cristae arrangement and swollen mitochondia in renal tubular epithelial cells. The atherosclerotic plaque was ruptured in groups B and C, and greater tubulointerstitial injury was noted with markedly decreased PTC density than group A2 (P<0.01).      Conclusion    The ARAS model we established is steady, credible, and easily repeated.

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更新日期/Last Update: 2008-07-15