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首页> 外文期刊>Journal of Medical Sciences >Biomarkers of Oxidative Stress of Sciatic Nerve Tissues in Experimental Diabetic Neuropathy
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Biomarkers of Oxidative Stress of Sciatic Nerve Tissues in Experimental Diabetic Neuropathy

机译：实验性糖尿病性神经病中坐骨神经组织氧化应激的生物标志物

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Oxidative stress resulting from enhanced free radical formation and/or a defect in antioxidant defenses has been implicated in the pathogenesis of experimental diabetic neuropathy. In the present study, we have investigated the effect of α-lipoic acid a potent free radical scavenger on glycemic control, oxidative stress and antioxidant enzymes of sciatic nerve in streptozotocin (STZ)-induced diabetic neuropathy model in rats. This study was carried out on 120 male rats. All rats were divided into six main equal groups, 20 animals each. Group 1 (control group) received no drugs, group 2 (diabetic group) received a single dose of streptozotocin (STZ) (50 mg kg-1 i.p.) for the induction of diabetes, group 3 (normal α-lipoic acid-treated group), group 4 (diabetic alpha-lipoic acid-treated group), group 5 (diabetic insulin-treated group), group 6 (diabetic alpha-lipoic acid and insulin-treated group). Eight weeks after diabetes induction therapeutic treatment with α-lipoic acid (54 mg kg-1 b.wt. i.p., daily) and insulin (2 U s.c daily) were given either alone or in combination and continued for six weeks. Equivalent volumes of saline were given subcutaneously to the rats in the other diabetic and non diabetic control groups. Blood samples and sciatic nerve tissues were collected from all animal groups two times at 4 and 6 weeks from the onset of treatment for determination of serum glucose and nitric oxide in addition to sciatic nerve L-malondialdehyde (L-MDA) and antioxidant enzymes (SOD, CAT and GPX) activities. The obtained results revealed that, a significant increase in serum glucose, sciatic nerve L-MDA concentrations and GPX activity with marked reduction in SOD and CAT activities were observed in STZ-induced diabetic neuropathy in rats. Treatment with alpha lipoic acid, insulin and their combination significantly decreased serum glucose and sciatic nerves L-MDA concentrations and significantly increased serum nitric oxide concentration as well as sciatic nerve SOD, CAT and GPX activities. These results suggest that, α-lipoic acid treatment with insulin improved significantly the diabetes-induced deterioration and attenuates the status of antioxidant enzymes and biomarkers of oxidative stress produced by diabetic neuropathy and its complication in diabetes mellitus.
机译：由增强的自由基形成和/或抗氧化剂防御缺陷引起的氧化应激与实验性糖尿病性神经病的发病机理有关。在本研究中，我们研究了α-硫辛酸（一种有效的自由基清除剂）在链脲佐菌素（STZ）诱导的糖尿病性神经病模型中对坐骨神经的血糖控制，氧化应激和抗氧化酶的影响。在120只雄性大鼠上进行了这项研究。将所有大鼠分成六个主要的相等组，每组20只动物。第一组（对照组）未服用任何药物，第二组（糖尿病组）仅接受一剂链脲佐菌素（STZ）（50 mg kg -1 ip）用于诱导糖尿病，第三组（正常） α-硫辛酸治疗组），第4组（糖尿病α-硫辛酸治疗组），第5组（糖尿病胰岛素治疗组），第6组（糖尿病α-硫辛酸和胰岛素治疗组）。糖尿病诱导后八周，单独或联合给予α-硫辛酸（每天54 mg kg -1 b.wt. ip）和胰岛素（每天2 U sc）进行治疗，并继续六个星期。在其他糖尿病和非糖尿病对照组中，皮下给予大鼠等量的盐水。在开始治疗的第4周和第6周，从所有动物组中两次采集血样和坐骨神经组织，以测定除坐骨神经L-丙二醛（L-MDA）和抗氧化酶（SOD）之外的血清葡萄糖和一氧化氮，CAT和GPX）活动。获得的结果表明，在STZ诱导的糖尿病性神经病大鼠中，血清葡萄糖，坐骨神经L-MDA浓度和GPX活性显着增加，而SOD和CAT活性显着降低。用α硫辛酸，胰岛素及其组合治疗可显着降低血清葡萄糖和坐骨神经的L-MDA浓度，并显着增加血清一氧化氮浓度以及坐骨神经的SOD，CAT和GPX活性。这些结果表明，用胰岛素对α-硫辛酸进行治疗可显着改善糖尿病引起的恶化，并减弱糖尿病性神经病及其并发症引起的抗氧化酶和氧化应激生物标志物的状态。

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