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We found that FeIII-iminodiacetate (IDA), a novel iron-chelator, induced acute tubular injuries and lipid peroxidation to the same extent.
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| Cordyceps sinensis(CS)is a potent mitogen for spleen cell.We exami-ned the effect of CS on DNA synthesis in renal tubular cell,The effect of CS on tubu-lar cell expression Of mRNA encoding cell growth regulating protooncogene c-myc wasalso examined.￣3H-thymidine incorporation in tubular cell was stimulated after the abbit-ion of sera taken from rat fed with CS. Renal tubular cell responded to CS solutionwith a 2.2 fold increase in concentration of 50μg/ml.However,further increament of CSsolution... Cordyceps sinensis(CS)is a potent mitogen for spleen cell.We exami-ned the effect of CS on DNA synthesis in renal tubular cell,The effect of CS on tubu-lar cell expression Of mRNA encoding cell growth regulating protooncogene c-myc wasalso examined.￣3H-thymidine incorporation in tubular cell was stimulated after the abbit-ion of sera taken from rat fed with CS. Renal tubular cell responded to CS solutionwith a 2.2 fold increase in concentration of 50μg/ml.However,further increament of CSsolution to 75μg/ml induced an inhibition of cell proliferation.The mechanism of itsbiphasic effect remained unexplored.CS(5μg/ml)upregulated c-myc mRNA expressionwithin 30 minutes and the effect was substained for 4 hours,which suggested an inter-ference in cell growth by pathways associated with modulation of the c-myc mechanism. It was demonstrated previously that the adminstration of mitogen for renal tubularcell,like EGF and TGF-α,accelerated the regencration of tubular cell after acute tubu-lar injury.To investigate whether there exists an associated responsiveness in CS. westudied renal function and recovery of tubular damage in acute gentamicin nephrotoxicmodel of rat,The use of CS prompted an earlier recovery from acute tubular injury ascompard with control.Thus,both in vitro and in vivo studies proved that CS is amitogen for tubular cell and it may be a herb of value in treatment of acute renalfailure. | 本研究证明冬虫夏草对体外培养的大鼠肾小管上皮细胞增殖具有明显促进作用，其增殖效应的机制可能与诱导肾小管细胞持续高水平地表达ｃ－ｍｙｃ原癌基因ｍＲＮＡ有关，鉴于急性肾衰治疗的中心环节正在于如何促进损伤、坏死的肾小管细胞再生、修复，因而推测虫草的上述作用可能对于急性肾衰治疗有益，采用虫草治疗庆大霉素诱发的大鼠急性肾损伤，确实具有良好的效果。 | Objective: To investigate the apoptosis in injury and regeneration of tubular epithelial cells.Methods: Acute and chronic renal tubular injury in female Wistar rats were induced by intraperitoneally injecting Gentamicin, and sacrificed at different time. Apotosis of rat tubular cells in primary cultures was induced by adding Gentamicin in different concentration. Apoptosis of renal tubular cells was detected with TUNEL technique and DNA agarose gel electrophoresis. The... Objective: To investigate the apoptosis in injury and regeneration of tubular epithelial cells.Methods: Acute and chronic renal tubular injury in female Wistar rats were induced by intraperitoneally injecting Gentamicin, and sacrificed at different time. Apotosis of rat tubular cells in primary cultures was induced by adding Gentamicin in different concentration. Apoptosis of renal tubular cells was detected with TUNEL technique and DNA agarose gel electrophoresis. The levels of cell proliferation were measured by displaying PCNA. The morphological changes in tubular cells were observed with electron microscopy.Results: Acute tubular injury showed that more cells exhibited necrosis and a few apoptosis. Chronic tubular injury showed mainly cellular degeneration and aoptesis. Apoptosis occured at two phases: associated necrosis phase and saiated regenerative phase. Conclusion: These data suggested Gentamicin in high concentration induced tubular cells necrosis, but that in low concentration induced tubular cells apoptosis and degeneration.Apoptosis plays an important role in remedification of regenerative tubule. | 阐明肾小管上皮细胞损伤及再生过程中细胞凋亡的意义。方法：给Wistar大鼠腹腔注射庆大霉素，分别造成急性和慢性肾小管损伤模型，不同时间宰杀。用原位末端标记法及DNA琼脂糖凝胶电泳观察细胞凋亡，增殖细胞核抗原（PCNA）免疫组化观察增殖情况。将不同浓度的庆大霉素加入培养的大鼠肾小管上皮细胞诱导凋亡。结果：大剂量庆大霉素主要造成肾小管上皮细胞坏死，少量细胞凋亡。小剂量庆大霉素长时间作用以空泡变性、凋亡为主。各个时间点后者的凋亡细胞数均高于前者。肾小管上皮细胞第5天出现再生，第9天达高峰，细胞凋亡于第5天出现第一个高峰，第12天出现第二个高峰，发生于再生高峰之后。体外实验中，小剂量庆大霉素引起较多细胞凋亡，大剂量庆大霉素主要引起细胞坏死。结论：大剂量庆大霉素造成肾小管上皮损伤以坏死为主，小剂量庆大霉素造成肾小管上皮细胞损伤以变性、凋亡为主。凋亡在肾小管上皮细胞再生过程中，有重要的修饰和改建作用。 | Objective To evaluate the protective effect of captopril(CAP) on acute renal ischemia-reperfusion injury in rabbits. Methods Model of acute renal ischemia-reperfusion injury was induced with the right suprarenal abdominal aorta being occlused for 30min then unclamped for 180 min. 24 rabbits were randomly divided into false operating group (A, n = 8), ischemia-reperfusion group (B, n = 8), and CAP-group (C, n = 8). In group C, CAP 2mg.kg~(-1) was given intravenously 5min prior to clamping... Objective To evaluate the protective effect of captopril(CAP) on acute renal ischemia-reperfusion injury in rabbits. Methods Model of acute renal ischemia-reperfusion injury was induced with the right suprarenal abdominal aorta being occlused for 30min then unclamped for 180 min. 24 rabbits were randomly divided into false operating group (A, n = 8), ischemia-reperfusion group (B, n = 8), and CAP-group (C, n = 8). In group C, CAP 2mg.kg~(-1) was given intravenously 5min prior to clamping and infused at a rate of 0.5mg. kg(-1). h(-1) for 15min. Other groups of rabbits received normal saline as controls,but the abdominal aorta was not occlused in group A. The parameters, including BUN, Cr, SOD, MDA, AT-Ⅱ and β_2-MG, were observed before, during ischemia and after reperfusion. The kidney specimens were examined using light and electron microscopy' Results In group C renal cortex and serum MDA,AT-Ⅱ concentration after reperfusion were significantly decreased (P＜0.01),SOD activity increased significantly (P<0.01) and serum BUN,Cr,urine β_2-MG levels decreased markedly compared with those in group B (P<0. 05 or P<0.01 )' The Paller's score for acute renal tubular injury was evidently lower in group C than that of group B (25. 00±7. 56 vs 82. 50±16. 69,P<0.05)' Under electron microscopy,renal pathology associated with acute tubular injury and necrosis were observed in group B, meanwhile, it was obviously alleviated in group C' Conclusion Captopril can effectively protect rabbit kidneys against ischemia-reperfusion injury during suprarenal abdominal aortic crossclaming. | 目的 探讨卡托普利（ＣＡＰ）对家兔肾上腹主动脉阻断致急性肾缺血／再灌注损伤（ＡＲＩＲＩ）的保护效果。方法 于肾上阻断腹主动脉血流３０ｍｉｎ再灌注１８０ｍｉｎ的方法制成双侧ＡＲＩＲＩ动物模型，将２４只家兔随机等分为假手术组（Ａ组）、缺血再灌注组（Ｂ组）和ＣＡＰ治疗组（Ｃ组）。Ｃ组于阻断主动脉前 ５ｍｉｎ静注 ＣＡＰ２ｍｇ· ｋｇ~（－１），继之持续输注 １５ｍｉｎ ＣＡＰ ０．５ｍｇ· ｋｇ~（－１）· ｈ~（－１）。 Ａ、Ｂ组以等容积生理盐水取代ＣＡＰ，Ａ组不阻断主动脉血流。动态检测血中ＢＵＮ、Ｃｒ、ＳＯＤ、ＭＤＡ、ＡＴ－Ⅱ，尿β_２－ＭＧ变化，以及肾皮质中ＳＯＤ、ＭＤＡ、ＡＴ－Ⅱ和肾组织形态学改变。结果 Ｃ组在再灌期血和肾皮质中ＭＤＡ、ＡＴ－Ⅱ浓度明显低于Ｂ组（Ｐ＜０．０１），ＳＯＤ活性显著高于Ｂ组（Ｐ＜０．０１），血ＢＵＮ、Ｃｒ及尿中β２－ＭＧ含量明显低于Ｂ组（Ｐ＜０．０５，＜０．０１）。Ｃ组光镜下肾小管损伤Ｐａｌｌｅｒ评分明显低于Ｂ组（２０．５０±７．５６ｖｓ ８２．５０±１６．６９，Ｐ＜０．０５），Ｂ组电镜见明显急性肾小管损伤及坏死，而Ｃ组肾小管损伤轻微。结论ＣＡＰ对家兔肾上腹主动脉阻断所致ＡＲＩＲＩ... 目的 探讨卡托普利（ＣＡＰ）对家兔肾上腹主动脉阻断致急性肾缺血／再灌注损伤（ＡＲＩＲＩ）的保护效果。方法 于肾上阻断腹主动脉血流３０ｍｉｎ再灌注１８０ｍｉｎ的方法制成双侧ＡＲＩＲＩ动物模型，将２４只家兔随机等分为假手术组（Ａ组）、缺血再灌注组（Ｂ组）和ＣＡＰ治疗组（Ｃ组）。Ｃ组于阻断主动脉前 ５ｍｉｎ静注 ＣＡＰ２ｍｇ· ｋｇ~（－１），继之持续输注 １５ｍｉｎ ＣＡＰ ０．５ｍｇ· ｋｇ~（－１）· ｈ~（－１）。 Ａ、Ｂ组以等容积生理盐水取代ＣＡＰ，Ａ组不阻断主动脉血流。动态检测血中ＢＵＮ、Ｃｒ、ＳＯＤ、ＭＤＡ、ＡＴ－Ⅱ，尿β_２－ＭＧ变化，以及肾皮质中ＳＯＤ、ＭＤＡ、ＡＴ－Ⅱ和肾组织形态学改变。结果 Ｃ组在再灌期血和肾皮质中ＭＤＡ、ＡＴ－Ⅱ浓度明显低于Ｂ组（Ｐ＜０．０１），ＳＯＤ活性显著高于Ｂ组（Ｐ＜０．０１），血ＢＵＮ、Ｃｒ及尿中β２－ＭＧ含量明显低于Ｂ组（Ｐ＜０．０５，＜０．０１）。Ｃ组光镜下肾小管损伤Ｐａｌｌｅｒ评分明显低于Ｂ组（２０．５０±７．５６ｖｓ ８２．５０±１６．６９，Ｐ＜０．０５），Ｂ组电镜见明显急性肾小管损伤及坏死，而Ｃ组肾小管损伤轻微。结论ＣＡＰ对家兔肾上腹主动脉阻断所致ＡＲＩＲＩ有良好的保护? | | | | << 更多相关文摘 |
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acute tubular injuries
急性肾小管损伤
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