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Estrogen receptor-beta ligand treatment after disease onset is neuroprotective in the multiple sclerosis model

机译:疾病发作后的雌激素受体-β配体治疗在多发性硬化症模型中具有神经保护作用

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摘要

Multiple Sclerosis (MS) is an autoimmune disease characterized by inflammation and neurodegeneration. Current MS treatments were designed to reduce inflammation in MS, rather than to directly prevent neurodegeneration. Estrogen has well-documented neuroprotective effects in a variety of disorders of the CNS, including experimental autoimmune encephalomyelitis (EAE), the most widely used mouse model of MS. Treatment with an estrogen receptor-beta (ERβ) ligand is known to effectively ameliorate clinical disease and provide neuroprotection in EAE. However, the protective effects of this ERβ ligand have only been demonstrated when administered prior to disease (prophylactically). Here, we tested whether ERβ ligand treatment could provide clinical protection when treatment was initiated after onset of disease (therapeutically). We found that therapeutic treatment effectively ameliorated clinical disease in EAE. Specifically, ERβ ligand-treated animals exhibited preserved axons and myelin as compared to vehicle treated animals. We observed no difference in the number of T lymphocytes, macrophages, or microglia in the CNS of vehicle versus ERβ ligand-treated animals. Our findings show that therapeutically administered ERβ ligand successfully treats clinical EAE, bearing translational relevance to MS as a candidate neuroprotective agent.
机译:多发性硬化症(MS)是一种以炎症和神经变性为特征的自身免疫性疾病。当前的MS治疗旨在减轻MS的炎症,而不是直接预防神经退行性变。雌激素在多种中枢神经系统疾病中具有公认的神经保护作用,包括实验性自身免疫性脑脊髓炎(EAE),这是最广泛使用的MS小鼠模型。已知用雌激素受体-β(ERβ)配体进行治疗可有效改善临床疾病并在EAE中提供神经保护作用。但是,仅在疾病发生前(预防性)给予该ERβ配体的保护作用。在这里,我们测试了疾病发作后开始治疗时,ERβ配体治疗是否可以提供临床保护。我们发现治疗有效地改善了EAE中的临床疾病。具体而言,与媒介物处理的动物相比,ERβ配体处理的动物表现出保存的轴突和髓磷脂。我们观察到与ERβ配体治疗的动物相比,媒介物的CNS中的T淋巴细胞,巨噬细胞或小胶质细胞的数量没有差异。我们的发现表明,治疗性给药的ERβ配体可成功治疗临床EAE,与MS作为候选神经保护剂具有翻译相关性。

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