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目的探讨大鼠肾缺血再灌注所致急性肾损伤时细胞聚合糖性死亡与外源性凋亡。方法应用免疫印迹技术、免疫组织化学染色技术以及光学和电子显微镜技术对缺血60min再灌注24h的大鼠肾组织进行观察和分析。结果免疫印迹分析结果表明,与sham组比较肾缺血再灌注后(AKI组)肾组织PARP-1、caspase-3和TNFRα表达增强。PARP-1、caspase-3免疫组化染色阳性细胞出现在缺血再灌注损伤肾组织,主要分布于肾小管,皮质和髓质外带的肾小管出现了大面积细胞坏死,表现为细胞肿胀,空泡形成,崩解脱落。在髓质外带肾小管坏死细胞之间存在着较多的凋亡细胞,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。凋亡细胞皱缩,界限清楚,核染色质固缩边聚。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聚合糖性死亡和外源性凋亡。
Objective To investigate the effects of acute renal injury induced by renal ischemia-reperfusion on cell apoptosis and exogenous apoptosis in rats. Methods Immunohistochemistry, immunohistochemical staining and optical and electron microscopy were used to observe and analyze the rat renal tissue after ischemia 60 min and reperfusion 24 h. Results The results of Western blot analysis showed that the expression of PARP-1, caspase-3 and TNFRα in renal tissue increased after renal ischemia-reperfusion (AKI) compared with sham group. The positive cells of PARP-1 and caspase-3 immunohistochemical staining appeared in the renal tissue of ischemia-reperfusion injury, mainly in renal tubules, cortex and medulla oblongata tubules appeared large area of cell necrosis, manifested as cell swelling, Cavitation formation, disintegration shedding. In medulla oblongata tubular necrosis cells there are more apoptotic cells, cell shrinkage, nuclear pyknosis. Electron microscope, necrotic cells swollen, organelles also swollen, collapse disappear. Apoptotic cells shrink, clear boundaries, nuclear chromatin shrinkage edge poly. Conclusions Polygalacturonase and extrinsic apoptosis occur in some renal tubular epithelial cells at 60 min after reperfusion for 60 min in rats.