大鼠缺血性肾损伤的细胞聚合糖性死亡与外源性凋亡

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。

Parthanatos and exogeneous apoptosis caused by ischemic injury in kidney of rats

Objective To explore the parthanatos and exogeneous apoptosis caused by acute ischemia kidney injury（AKI） in rats. Immunoblot analysis, immunohistochemical staining, and light and electron microscope were used in this study. Results Immunoblot analysis proved that expression levels of polyADP-ribose polymerase-1（PARP-1）, caspase-3 and tumor necrosis factor receptor α （TNFR or） were significantly higher in AKI animals than in sham. PARP-1 and caspase-3 positive cells were located in renal tubules with evident necrosis in both cortical and outer region of medulla after 60min ischemia and 24h reperfusion, but apoptosis tubule cells were found only in the outer region of medulla in AKI animal kidneys. Condusion Ischemia reperfusion caused parthanatos and exogenous apoptosis of renal tubular cells of rats.