摘要
目的观察大鼠缺血性急性肾损伤对其肝细胞形态学的影响。方法健康SD大鼠30只被分为假手术组(sham)、缺血性急性肾损伤组(IAKI)和双肾切除组(BNx),每组10只。成功制造IAKI模型后24 h经颈总动脉取血进行肾功能和肝功能检测;采用光学显微镜、电子显微镜技术观察缺血性急性肾损伤大鼠的肝脏形态学变化;分别采用免疫组织化学和免疫印迹方法检测IAKI大鼠肝脏多聚二磷酸腺苷核糖聚合酶-1(PARP-1)和Caspase-3蛋白的表达情况。结果缺血性急性肾损伤的动物发生了急性肝损伤,肝功能受损。肝脏出现了大小不等坏死病灶。肝细胞损伤的形态学分类包括苍白样坏死、空泡样坏死,固缩性死亡以及细胞凋亡,其中细胞坏死多见。免疫印迹和免疫组织化学染色结果显示,IAKI诱导的肝细胞受损过程中PARP-1和Caspase-3被激活。结论缺血性急性肾损伤可引起肝细胞坏死和凋亡,但以细胞坏死为主。PARP-1介导细胞死亡、Caspase依赖细胞死亡均参与了IAKI诱导的肝细胞损伤。
Objective To observe morphological effects of ischemic acute kidney injury （IAKI） on hepatocytes in rats. Methods Western blotting, immunohistochemical staining, light and electron microscopy were used in this observation. Results Necrotic lesions, including pale and vacuolization necrosis lesions, in varied sizes were found in livers of IAKI animals. Cytologically, hepatocyte with either pale necrosis or vacuolization necrosis, hepatocytes with pyknotic cell death and undergoing apoptosis constituted the hepatic damages induced by IAKI but necrosis was more evident. Western blotting assays provided that both PARP-1 and Caspase-3 expressed much stronger in livers of IAKI animals. In addition immunohistochemical staining of both PARP-1 and Caspase-3 revealed that positive hepatocytes were more evident during the acute hepatic damage induced by IAKI. Conclusion Necrosis, PARP-1 mediated cell death and apoptosis, Caspase-dependent cell death are involved in hepatic damages induced by IAKI, but necrosis is more predominated.
出处
《解剖学报》
CAS
CSCD
北大核心
2012年第5期635-640,共6页
Acta Anatomica Sinica
基金
辽宁医学院归国人员启动基金资助项目(Y20101311)
