摘要
目的:观察大鼠急性肾损伤(AKI)引起肝细胞凋亡的细胞学特点。方法:建立AKI(包括缺血性和非缺血性)大鼠模型后应用免疫印迹法、免疫组织化学染色法和光学、电子显微镜技术对AKI大鼠的肾脏和肝脏进行观察。结果:(1)缺血性AKI肾小管出现了大面积细胞坏死和细胞凋亡的表现。不论是缺血性还是非缺血性AKI的动物都发生了急性肾功能损伤和急性肝功能受损。(2)免疫印迹法测定结果显示AKI动物肝脏的肿瘤坏死因子受体α(TNFRα)和半胱氨酸天冬氨酸蛋白酶-3(caspase-3)蛋白表达增强。从caspase-3免疫组化染色的结果可以看出阳性细胞均出现在AKI动物肝脏内。(3)电子显微镜观察发现AKI动物肝脏中确有细胞凋亡和副凋亡的表现。(4)缺血性与非缺血性AKI诱导肝细胞凋亡的表现相同。结论:AKI可引起肝细胞凋亡和副凋亡,其中经TNFRα启动的caspase依赖的细胞死亡构成了AKI引起的肝细胞凋亡。这种肝细胞凋亡是由肾功能损伤导致的血尿毒物质引起的。
AIM ： To observe the cytological changes of hepatocytes undergoing apoptosis induced by acute kid- ney injury （AKI） in rats. METHODS： The rat models of AKI, including ischemic and non -isehemic AKI, were estab- lished. Western blotting, immunohistochemical staining, light and electron microscopy were used in this study. RE- SULTS： Cellular necrosis in renal tubules, as the basic morphological changes of ischemic AKI, and renal tubular cells undergoing apoptosis were evident in ischemic AKI. Meanwhile, tumor necrosis facotor receptor α （TNFRα） and caspase - 3 was strongly expressed in the livers from AKI rats. Caspase -3 -positive cells were evident in the livers from AKI rats. Microscopic examinations revealed that hepatocytes undergoing apoptosis and para - apoptosis were observed in damaged livers of both ischemic and non - ischemic AKI animals. No significant difference of hepatic apoptosis between ischemic and non - ischemic AKI animals was observed. CONCLUSION： Either apoptosis, caspase - dependent cell death or para -apoptosis are involved in hepatic injury induced by AKI. TNFRα initiation and cleaved caspase family are the pathways of hepatocytes undergoing apoptosis induced by AKI.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2012年第12期2233-2237,共5页
Chinese Journal of Pathophysiology
基金
辽宁医学院归国人员启动基金资助项目(No.Y20101311)
