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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 the effect of ischemic acute kidney injury on morphology of hepatocytes in rats. Methods Thirty healthy SD rats were divided into sham group, IAKI group and BNx group, with 10 in each group. Twenty-four hours after the successful establishment of IAKI model, the carotid artery was taken for renal and liver function test. The morphological changes of liver in ischemic acute renal injury rats were observed by optical microscope and electron microscope. Immunohistochemistry and immunohistochemistry Western blotting was used to detect the expression of PARP-1 and Caspase-3 protein in IAKI rat liver. Results The animals with ischemic acute kidney injury developed acute liver injury and impaired liver function. Liver appeared in varying sizes necrosis lesions. Morphological classification of liver cell damage include pale-like necrosis, vacuolar necrosis, shrinkage death and apoptosis, of which cell necrosis is more common. Immunoblotting and immunohistochemical staining revealed that PARP-1 and Caspase-3 were activated during IAKI-induced hepatocellular injury. Conclusion Ischemia-induced acute kidney injury can cause necrosis and apoptosis of hepatocytes, but the main cell necrosis. PARP-1-mediated cell death, Caspase-dependent cell death are all involved in IAKI-induced hepatocellular injury.