Kashani Iraj Ragerdi, Chavoshi Hossein, Pasbakhsh Parichehr, Hassani Mahmoud, Omidi Ameneh, Mahmoudi Reza, Beyer Cordian, Zendedel Adib
Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Department of Medical Nanotechnologies, School of Advanced Technologies, Tehran University of Medical Sciences, Tehran, Iran.
Iran J Basic Med Sci. 2017 Aug;20(8):886-893. doi: 10.22038/IJBMS.2017.9110.
Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of multiple sclerosis. The aim of the present work is to investigate the protective effects of erythropoietin against cuprizone-induced oxidative stress.
Adult male C57BL/6J mice were fed a chow containing 0.2 % cuprizone for 6 weeks. After 3 weeks, mice were simultaneously treated with erythropoietin (5,000 IU/kg body weight) by daily intraperitoneal injections.
Our results showed that cuprizone induced oxidative stress accompanied with down-regulation of subunits of the respiratory chain complex and demyelination of corpus callosum. Erythropoietin antagonized these effects. Biochemical analysis showed that oxidative stress induced by cuprizone was regulated by erythropoietin. Similarly, erythropoietin induced the expression of subunits of the respiratory chain complex over normal control values reflecting a mechanism to compensate cuprizone-mediated down-regulation of these genes.
The data implicate that erythropoietin abolishes destructive cuprizone effects in the corpus callosum by decreasing oxidative stress and restoring mitochondrial respiratory enzyme activity.
越来越多的实验和临床研究证据表明，氧化应激在多发性硬化症的发病机制中起主要作用。本研究的目的是探讨促红细胞生成素对铜离子螯合剂诱导的氧化应激的保护作用。
成年雄性C57BL/6J小鼠喂食含0.2%铜离子螯合剂的食物6周。3周后，小鼠同时每天腹腔注射促红细胞生成素（5000 IU/kg体重）。
我们的结果表明，铜离子螯合剂诱导氧化应激，同时伴有呼吸链复合物亚基的下调和胼胝体脱髓鞘。促红细胞生成素拮抗了这些作用。生化分析表明，铜离子螯合剂诱导的氧化应激受促红细胞生成素调节。同样，促红细胞生成素诱导呼吸链复合物亚基的表达超过正常对照值，反映了一种补偿铜离子螯合剂介导的这些基因下调的机制。
数据表明，促红细胞生成素通过降低氧化应激和恢复线粒体呼吸酶活性，消除了铜离子螯合剂对胼胝体的破坏作用。
