摘要
目的观察大鼠缺血性急性肾损伤对海马CA1区神经元的形态学影响。方法成功制造缺血性急性肾损伤大鼠模型后应用光镜电镜技术观察海马CA1区形态学变化,应用免疫组织化学及免疫印迹技术对海马组织中聚二磷酸腺苷核糖聚合酶-1(PARP-1)和caspase-3的表达进行定位观察和定量检测分析。结果肾缺血60 min再灌注24 h后光镜下海马CA1区锥体细胞层出现了固缩性神经元,经电子显微镜观察发现细胞萎缩,基质电子密度增高,细胞核萎缩但无染色质固缩表现,内质网扩张、线粒体肿胀变性。免疫组化染色及免疫印迹结果显示缺血性急性肾损伤的海马caspase-3阴性表达,而PARP-1表达明显增强。结论大鼠缺血性急性肾损伤可引起海马CA1区锥体细胞层神经元固缩性损伤,即细胞质性死亡,推测这种损伤可能属于PARP-1介导的细胞死亡。
Objective To observe morphological changes of hippocampal CA1 neurons induced by ischemic acute kidney injury （IAKI） in rats.Methods After successful preparation of rat model of IAKI, the morphological changes of hip-pocampal CA1 neurons were observed by light microscope and electron microscope. The expressions of polyADP-ribose polymerases （PARP）-1 and caspase-3 in hippocampal CA1 neurons were detected by immunohistochemical （IHC） staining and Western blot assay.Results Pyknotic neurons in hippocampal CA1 area were found after 60 min ischemia and 24 h re-perfusion in kidney. Results of electron microscope showed that swollen mitochondria and dilated endoplasmic reticule in cy-toplasm and shrinkage nucleus with no pyknotic chromatin in the pyknotic neurons. IHC staining showed the negative cas-pase-3 staining and positive PARP-1 staining in pyknotic neurons. Conclusion The pyknotic neurons induced by IAKI might be mediated by PARP-1.
出处
《天津医药》
CAS
北大核心
2014年第2期164-166,I0003,共4页
Tianjin Medical Journal
基金
辽宁省自然科学基金资助项目(项目编号:201202141,201102139)
辽宁医学院博士启动基金(项目编号:20101311)
