引用本文:刘玉玲,包翠芬,邵佑之.大鼠双侧肾切除后肝细胞的损伤方式[J].重庆医科大学学报,2014,38(6):781~785
大鼠双侧肾切除后肝细胞的损伤方式
Damage modes of hepatocytes after bilateral nephrectomy in rats
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中文关键词:  非缺血性急性肾损伤  双侧肾切除  肝细胞  坏死  PARP-1介导的细胞死亡  凋亡  caspase依赖的细胞死亡
英文关键词:non ischemic acute kidney injury  bilateral nephrectomy  hepatocyte  necrosis  PARP-1 mediated cell death  apoptosis  caspase dependent cell death
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刘玉玲,包翠芬,邵佑之 辽宁医学院科学实验中心辽宁 121000 
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中文摘要:
      目的:观察大鼠双侧肾切除[非缺血性急性肾损伤(non ischemic acute kidney injury,NIAKI)]引起肝细胞损伤方式。方法:应用Western blot、免疫组织化学染色方法和光学、电子显微镜技术对双侧肾切除24 h后的大鼠肝脏进行了观察。结果:双侧肾切除24 h后的大鼠发生了急性肝功能受损,肝脏出现了大小不等坏死灶以及大面积区域性肝细胞的空泡样改变。光、电镜观察结果证明前者以细胞坏死为主,后者以细胞内出现大量空泡为主要表现。此外尚可见少许肝细胞凋亡的表现。Western blot的结果说明双侧肾切除后肝脏内多聚ADP核糖聚合酶(polyADP-ribose polymerase,PARP)-1过度激活,肿瘤坏死因子受体1和caspase-3蛋白表达均增强。免疫组化染色结果可见双侧肾切除后肝脏内出现了PARP-1阳性和 caspase-3阳性的肝细胞。结论:形态学上NIAKI可引起肝细胞坏死,肝细胞空泡化与细胞凋亡,以前2种损伤为明显。从生物化学角度可以看出 PARP-1介导的细胞死亡与caspase依赖的细胞死亡参与了NIAKI引起的急性肝损伤。
英文摘要:
      Objective:To observe the morphological changes of hepatocyte injury induced by bilateral nephrectomy due to non ischemic acute kidney injury(NIAKI). Methods:Western blot,immunohistochemical staining,light and electron microscopy were used in this observation at 24 h after bilateral nephrectomy. Results:Acute liver damage was observed at 24 h after bilateral nephrectomy. Necrotic and vacuolization lesions were predominately evident in damaged livers after nephrectomy. Besides necrosis,hepatocytes with vac-uolization was also observed under electron microscopes. Meanwhile,polyADP-ribose polymerase-1(PARP-1),tumor necrosis factor receptor 1 and caspase-3 were expressed much stronger in NIAKI associated livers by Western blot analysis. Immunohistochemical staining demonstrated that PARP-1 positive nucleuses and caspase-3 positive cells were observed in the acute hepatic injury induced by nephrectomy. Conclusion:NIAKI can induce necrosis,apoptosis and vacuolation of liver cells,more evident in necrosis and apop-tosis,based on morphological observation. PARP mediated cell death and caspase-dependent cell death are involved in NIAKI asso-ciated hepatic damages.
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