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首页> 外文期刊>Neurobiology of disease >Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model
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Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model

机译：在鼠MOG诱发的多发性硬化症模型中，氯喹醇对铜/锌的螯合可减少脊髓白质损伤和行为缺陷

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摘要

The present study aimed to evaluate the therapeutic potential of clioquinol (CQ), a metal chelator, on multiple sclerosis pathogenesis. Experimental autoimmune encephalomyelitis was induced by immunization with myelin oligodendrocyte glycoprotein (MOG(35-55)) in female mice. Three weeks after the initial immunization, demyelination and immune cell infiltration in the spinal cord were analyzed. CQ (30. mg/kg) was given by gavage once per day for the entire experimental course. CQ profoundly reduced the daily clinical score and incidence rate of EAE mice. The CQ-mediated inhibition of the clinical course of EAE was accompanied by suppression of demyelination and reduced infiltration by encephalitogenic immune cells including CD4, CD8, CD20 and F4/80 positive cells. CQ also remarkably inhibited EAE-associated BBB disruption and MMP-9 activation. Autophagy contributes to clearance of aggregated proteins in astrocytes and neurons. The present study found that EAE increased the induction of autophagy and CQ further increased this expression. Furthermore, the present study found that post-treatment with CQ also reduced the clinical score of EAE and spinal cord demyelination. These results demonstrate that CQ inhibits the clinical features and neuropathological changes associated with EAE. The present study suggests that transition metals may be involved in several steps of multiple sclerosis pathogenesis.
机译：本研究旨在评估金属螯合剂氯喹诺醇（CQ）对多发性硬化症发病机理的治疗潜力。实验性自身免疫性脑脊髓炎是通过在雌性小鼠中用髓磷脂少突胶质细胞糖蛋白（MOG（35-55））进行免疫来诱导的。初次免疫后三周，分析脊髓中的脱髓鞘和免疫细胞浸润。在整个实验过程中每天通过管饲法给予CQ（30. mg / kg）。 CQ极大地降低了EAE小鼠的日常临床评分和发病率。 CQ介导的对EAE临床病程的抑制伴随着脱髓鞘的抑制和包括CD4，CD8，CD20和F4 / 80阳性细胞在内的致脑炎性免疫细胞的浸润减少。 CQ还显着抑制了与EAE相关的BBB破坏和MMP-9激活。自噬有助于清除星形胶质细胞和神经元中聚集的蛋白质。本研究发现EAE增加了自噬的诱导，而CQ进一步增加了该表达。此外，本研究发现，CQ后处理还降低了EAE和脊髓脱髓鞘的临床评分。这些结果表明，CQ抑制了与EAE相关的临床特征和神经病理学改变。本研究表明过渡金属可能参与多发性硬化症发病机制的几个步骤。

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