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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。
In this experiment, a method of intravenous injection of doxorubicin was used to make a model of rat nephrotic syndrome. Rat renal cortical lipid peroxidation malondialdehyde (MDA) peaked on the 8th day, 27.16 ± 4.36nmol / 100mg, serum MDA was significantly increased. Treatment of adriamycin nephropathy with active oxygen scavenger superoxide dismutase (O 2 - (-)), catalase (H 2 O 2) and dimethyl sulfoxide (scavenging · OH) (P <0.01), serum MDA decreased significantly (P <0.05 ~ 0.01), proteinuria decreased significantly (P <0.01), renal pathological changes also alleviated. Thus, reactive oxygen species in adriamycin nephropathy pathogenesis plays an important role.