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本文分别测定了正常对照组、糖尿病模型组，用不同剂量超氧化物歧化酶（ＳＯＤ）治疗糖尿病模型大鼠坐骨神经组织中总ＳＯＤ（Ｔ－ＳＯＤ）、铜锌ＳＯＤ（Ｃｕ－Ｚｎ－ＳＯＤ）、过氧化脂质（ＬＰＯ）、丙二醛（ＭＤＡ）水平。结果：糖尿病大鼠神经组织中ＬＰＯ、ＭＤＡ高于正常对照组；Ｔ－ＳＯＤ、Ｃｕ－Ｚｎ－ＳＯＤ水平则低于对照组（Ｐ＜０．０１）。大剂量ＳＯＤ比小剂量ＳＯＤ提高Ｔ－ＳＯＤ、Ｃｕ－Ｚｎ－ＳＯＤ，降低ＬＰＯ、ＭＤＡ作用明显。提示糖尿病神经组织中自由基代谢异常是导致糖尿病神经病的原因之一，而外源性ＳＯＤ对糖尿病神经组织中自由基有清除作用。
In this study, we measured the levels of total superoxide dismutase (T-SOD), Cu-Zn-SOD and Cu-Zn-SOD in the sciatic nerve tissue of diabetic rats and normal control group, diabetic model group and different doses of superoxide dismutase (SOD) Lipid peroxidation (LPO), malondialdehyde (MDA) levels. Results: The levels of LPO and MDA in nerve tissue of diabetic rats were higher than those in normal control group. The levels of T-SOD and Cu-Zn-SOD were lower than those in control group (P <0.01). High dose of SOD than low dose of SOD increased T-SOD, Cu-Zn-SOD, reduce LPO, MDA significantly. It is suggested that the abnormal metabolism of free radicals in diabetic nerve tissue is one of the reasons leading to diabetic neuropathy. Exogenous SOD has scavenging effect on free radicals in diabetic nerve tissue.