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作 者:王宁[1,2] 李郭锦[1,3] 刘霞[1] 包翠芬[1] 郭敏[1]
机构地区:[1]辽宁医学院组织胚胎学教研室,锦州121001 [2]盘锦市中心医院急诊科,盘锦124010 [3]辽宁医学院附属三院影像科,锦州121001
出 处:《中国体视学与图像分析》2013年第4期395-401,共7页Chinese Journal of Stereology and Image Analysis
基 金:辽宁省自然科学基金(201102139)
摘 要:目的探讨大鼠缺血再灌注损伤引起急性肾损伤的细胞死亡方式。方法应用光镜和电子显微镜技术、免疫组织化学染色及免疫印迹技术对缺血60 min再灌注24 h的大鼠肾脏进行了详细观察和分析。结果光镜可见皮质和髓质外带肾小管出现了①大面积细胞坏死:表现为细胞肿胀,空泡形成,崩解脱落;②坏死性凋亡:表现为细胞肿胀,核固缩;③细胞凋亡:分布于髓质外带肾小管坏死细胞之间,表现为细胞皱缩,核固缩。电镜下坏死细胞肿胀,细胞器也肿胀,崩解消失;凋亡细胞胞质皱缩,核染色质固缩边聚;坏死性凋亡呈坏死样细胞质含有一个凋亡样细胞核。免疫组化染色结果显示:PARP-1、RIPk3和caspase-3阳性细胞出现在缺血再灌注损伤肾组织内,主要分布于肾小管。免疫印迹分析结果表明:与Sham组比较肾缺血再灌注后肾组织PARP-1、RIPk3、caspase-3和TNFRa蛋白表达增强(P<0.05)。结论大鼠肾缺血60 min再灌注24 h部分肾小管上皮细胞发生了三种方式死亡,即聚合糖性死亡、坏死性凋亡和凋亡。Objective To observe the modes of cell death involved in acute ischemia-reperfusion injury of the kidneys in rats. Methods Light and electron microscopy, immunohistochemical staining and immunoblot analysis were used in this study. Results Renal tubular cells with necrosis and undergoing necroptosis were evident in both cortical and outer region ofthe medulla after 60 min ischemia and 24 h reperfusion. Tubular cells undergoing apoptosis were only found in the outer region of medulla in the injured rat kidneys. PARP-1-, RIPk3- and caspase-3-positive cells by IHC staining were evident in the injured rats, but negative in the sham animals. The results of immunoblot analysis provided that expressions of poly- ADP-ribose polymerase-1 ( PARP-1 ) , receptor interacting protein kinase 3 ( RIPk3 ) , caspase-3 and tumor necrosis factor receptor a (TNFRa) were significantly higher in the injured rats. Conclusions Renal tubular cells und and 24 h reperfusion ergoing parthanatos and necroptosis and apoptosis take place after 60 min ischemia in rat kidneys.
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