氧自由基及其清除剂SOD在阿霉素大鼠肾病模型中的作用  

THE ROLE FOR OXYGEN FREE RADICALS AND SUPEROXIDE DISMUTASE IN ADRIAMYCIN- INDUCED NEPHROTIC SYNDROME IN RATS

作　　者：甘华[1] 尹培达[1] 张仕光[1] 姜悦[1] 何柏林[1] 何惠娟[1] 胡媛芳[2] 

机构地区：[1]中山医科大学附属第一医院肾脏研究所 [2]中山医科大学病理学教研组

出　　处：《中山医科大学学报》1992年第2期40-44,共5页Academic Journal of Sun Yat-sen University of Medical Sciences

摘　　要：用阿霉素(ADR)诱导雄性大鼠肾病模型,选用氧自由基清除剂超氧化物歧化酶(SOD),以及非氧自由基清除剂环孢素A(CSA)对动物模型进行干扰,结果显示其模型组动物在实验的第14天出现典型肾病综合征症候;SOD组动物的尿,血生化指标及病理损害得到明显的改善,且血清和肾皮质的丙二醛(MDA)含量也明显低于ADR模型组的指标;CSA组则无上述作用,提示ADR能致使动物肾病模型是与氧自由基、脂质过氧化损伤有关。A single intravenous injection of adriamycin (ADR) results in marked protein uria, hypohlbutminemia, hypercholesteremia, ascites and glonerular morphological changes that are similar to minimal change disease in humans. We examined the effect of the superoxide ani-on[O2.] scavenger-superoxide dismutase (SOD) and non-oxygen free radicals scavenger-cyclo-sporin A (CSA) on ADR-induced nephrotic syndrome. The experiment found that the SOD can significantly reduce proteinuria, ameliorate serum biochemical index, and also attenuate renal injury. In particular, SOD also significantly suppress the serum and renal cortices malondialdehyde (MDA) concentration. Treatment with CSA was ineffective. The results suggest that the associated glomerular lesion in the ADR model is mediated by oxygen free radicals and lipid peroxides

关 键 词：阿霉素 氧自由基 肾病综合征 SOD 

分 类 号：R692.02[医药卫生—泌尿科学]