期刊文献+

急性肾缺血再灌注大鼠肾细胞游离钙水平与细胞凋亡的研究 被引量:1

Studies of both intracellular ionized calcium level and apoptosis during acute renal ischemic reperfusion injury
下载PDF
导出
摘要 目的观察缺血再灌注损伤对肾细胞游离钙([Ca2+]i)水平和细胞凋亡的影响。方法采用摘除左肾,钳夹大鼠右侧肾蒂,建立急性缺血再灌注肾损伤模型,应用Fura-2/AM荧光指示剂测定缺血再灌注大鼠肾细胞[Ca2+]i水平,流式细胞术检测肾细胞凋亡率。结果缺血再灌注不同时期肾细胞呈现不同程度Ca2+超载,与对照组相比差异显著(P<0.01);肾细胞凋亡率增高,与对照组相比差异显著(P<0.05、P<0.01),有正相关趋势。结论缺血再灌注不同时期肾细胞游离钙([Ca2+]i)水平增高,并与肾细胞凋亡率有正相关趋势,再灌注时间与肾细胞Ca2+超载呈正相关,提示再灌注损伤在加重细胞钙超载同时增加了肾组织细胞凋亡,可能是再灌注损伤肾功能障碍的重要原因。 Objective Effects of renal ischemic reperfusion injury on intracellular inonized calcium level and apoptosis are observerd.Methods The model of rat's acute renal ischemic reperfusion injury was established by both cutting the left kidney and occlusing right kidney pedicle.The renal intracellular i level and the renal cell apoptosis were measured by using Fura-2/AM fluorescence assay and flow cytometry respectivly.Results Compared with the control group,renal intracellular [Ca^2+]i level increased significantely(P〈0.01) and apoptosis rate increased significantely(P〈0.05,P〈0.01) at different periods of ischemic reperfusion.Conclusion At different periods of rat's acute renal ischemic reperfusion injury,renal intracellular I rises and becomes postive relationship with the apoptosis rate.There is positive relevent between the reperfusion time and renal intracellular i overloading.This may be important reason of renal disfunction due to reperfusion injury.
出处 《中国实验诊断学》 北大核心 2010年第7期999-1001,共3页 Chinese Journal of Laboratory Diagnosis
关键词 缺血再灌注 肾组织 细胞钙超载 细胞凋亡 ischemic reperfusion intracellular ionized calcium renal tissue apoptosis
  • 相关文献

参考文献7

  • 1Lario S,Mendes D,Bescos M,et al.Expression of transforming growth factor-beta1 and hypoxia-inducible factor-1alpha in an experimental model of kidney transplantation[J].Transplantation,2003,75(10):1647.
  • 2Salas MA,Valverde CA,Sánchez G,et al.The signalling pathway of CaMKII-mediated apoptosis and necrosis in the ischemia/reperfusion injury[J].J Mol Cell Cardiol,2010,48(6):1298.
  • 3Marciniak SJ,Ron D.Endoplasmic reticulum stress signaling in disease[J].Physiol Rev,2006,86(4):1133.
  • 4Boulares AH,Ren T.Mechanism of Acetaminophen-Induced Apoptosis in Cultured Cells:Roles of Caspase-3,DNA Fragmentation Factor,and the Ca2+ and Mg2+ Endonuclease DNAS1L3[J].Pharmacol Toxicol,2004,94(1):19.
  • 5傅耀文,张文岚,薛立娟.缺血再灌注对肾细胞内钙水平和细胞凋亡的影响[J].中华泌尿外科杂志,2004,25(12):834-837. 被引量:9
  • 6Li Z,Nickkholgh A,Yi X,et al.Melatonin protects kidney grafts from ischemia/reperfusion injury through inhibition of NF-kB and apoptosis after experimental kidney transplantation[J].J Pineal Res,2009,46(4):365.
  • 7Zhang GX,Kimura S,Murao K,et al.Inhibition of cytochrome c release by 10-N-nonyl acridine orange,a cardiolipin-specific dye,during myocardial ischemia-reperfusion in the rat[J].Am J Physiol Heart Circ Physiol,2010,298(2):H433.

二级参考文献6

  • 1Lario S, Mendes D, Bescos M, et al. Expression of transforming growth factor-beta1 and hypoxia-inducible factor-1alpha in an experimental model of kidney transplantation. Transplantation, 2003, 75: 1647-1654.
  • 2Boulares AH, Ren T. Mechanism of Acetaminophen-Induced apoptosis in cultured cells: roles of caspase-3, DNA fragmentation factor, and the Ca2 + and Mg2 + endonuclease DNAS1L3. Pharmacol Toxicol, 2004,94:19-29.
  • 3Schumer M, Colombel MC, Sawchuk TS, et al. Morphologic, biochemical and molecular evidence of apoptosis during in the reperfusion phase after brief periods of renal ischemia. Am J Phathol, 1992,140:831-834.
  • 4Raafat AM,Murray MT,McGuire T,et al. Calcium blockade reduces renal apoptosis during ischemia reperfusion. Shock, 1997,8:186-192.
  • 5Toronyi E, Hamar J, Perner F, et al. Prevention of apoptosis reperfusion renal injury by calcium channel blockers. Exp Toxicol Pathol,1999,51:209-212.
  • 6Burns AT, Davies DR, McLaren AJ, et al. Apoptosis in ischemia/reperfusion injury of human renal allografts. Transplantation, 1998,66:872-876.

共引文献8

同被引文献19

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部