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纸质出版:2007
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黄朝晖,吴雄飞,赵洪雯,刘宏,王汉民.ApoE-/-小鼠肾动脉狭窄及肾损害特点观察[J].陆军军医大学学报(原第三军医大学学报),2007,29(19):1844-1847.
HUANG Zhao-hui,WU Xiong-fei,ZHAO Hong-wen,LIU Hong,WANG Han-min.Atherosclerotic renal artery stenosis and renal injury in apolipoprotein E knockout mouse[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(19):1844-1847.
黄朝晖,吴雄飞,赵洪雯,刘宏,王汉民.ApoE-/-小鼠肾动脉狭窄及肾损害特点观察[J].陆军军医大学学报(原第三军医大学学报),2007,29(19):1844-1847. DOI:
HUANG Zhao-hui,WU Xiong-fei,ZHAO Hong-wen,LIU Hong,WANG Han-min.Atherosclerotic renal artery stenosis and renal injury in apolipoprotein E knockout mouse[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(19):1844-1847. DOI:
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A
1
(未破裂)和A
2
(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 A
1
组未发现其下游肾脏病理改变;②A
2
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A
2
组比较,差异显著(P0.01);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。
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 (A
1
: stable
A
2
: 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 A
1
. Obvious tubulointerstitial injury was noted in group A
2
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 A
2
(P0.01). Conclusion The ARAS model we established is steady
credible
and easily repeated.
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