摘要
本实验用阿霉素一次静注的方法,制作了大鼠肾病综合征的模型。大鼠肾皮质过氧化脂质丙二醛(MDA)在第8天达到高峰,为27.16±4.36nmol/100mg,血清MDA也明显升高。用活性氧清除剂超氧化物歧化酶(清除O_2^(·-))、过氧化氢酶(清除H_2O_2)、二甲基亚砜(清除·OH)治疗阿霉素肾病,可见肾皮质MDA显著减少(P<0.01),血清MDA也显著减少(P<0.05～0.01),蛋白尿明显降低(P<0.01),肾脏病理变化也减轻。由此可见,活性氧在阿霉素肾病的发病机制中起重要作用。
Whether oxygen free radicals contribute to the development of adriamycin (ADR) nephrosis is examined. Five groups of male SD rats were studied. The peak concentration of malondialdehyde (MDA) of kidney cortex, 27.16±4.36nmol/100mg, was found on 8th day after ADR treatment. ADR-treated rats received either superoxide dismutase (SOD), catalase (CAT) or dimethyl sulfoxide (DMSO). The SOD, CAT or DMSO treatment group had a significant suppression of proteinuria (P<0.01), serum and renal cortex MDA (P<0.05-0.01) compared to ADR control group. There were also less severe renal morphologic changes in former three groups vs. the ADR controls. These data provide indirect evidence that oxygen free radicals generated by ADR are important mediators of ADR-induced nephrosis.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第3期306-309,共4页
Chinese Journal of Pathophysiology
关键词
肾病综合征
阿霉素
游离基类
Free radicals
Adriamycin
Nephrosis
Malondialdehyde
