Institute of Anatomy and Cell Biology, Medical College, Zhejiang University, Hangzhou, China.
Department of Electrophysiology, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou, China.
Mediators Inflamm. 2018 Feb 18;2018:4187347. doi: 10.1155/2018/4187347. eCollection 2018.
Neuromyelitis optica (NMO) is an autoimmune inflammatory demyelinating disease that mainly affects the spinal cord and optic nerve, causing blindness and paralysis in some individuals. Moreover, NMO may cause secondary complement-dependent cytotoxicity (CDC), leading to oligodendrocyte and neuronal damage. In this study, a rodent NMO model, showing typical NMO pathogenesis, was induced with NMO-IgG from patient serum and human complement. We then tested whether the combination of C16, an v3 integrin-binding peptide, and angiopoietin-1 (Ang1), a member of the endothelial growth factor family, could alleviate NMO in the model. Our results demonstrated that this combination therapy significantly decreased disease severity, inflammatory cell infiltration, secondary demyelination, and axonal loss, thus reducing neural death. In conclusion, our study suggests a possible treatment that can relieve progressive blindness and paralysis in an animal model of NMO through improvement of the inflammatory milieu.
视神经脊髓炎（NMO）是一种自身免疫性炎症性脱髓鞘疾病，主要影响脊髓和视神经，导致部分患者失明和瘫痪。此外，NMO 可能导致补体依赖性细胞毒性（CDC），从而导致少突胶质细胞和神经元损伤。在这项研究中，我们使用来自患者血清的 NMO-IgG 和人补体诱导了一种具有典型 NMO 发病机制的啮齿动物 NMO 模型。然后，我们测试了 v3 整合素结合肽 C16 和血管生成素-1（Ang1）（内皮生长因子家族的一员）的组合是否可以缓解该模型中的 NMO。我们的结果表明，这种联合治疗可显著降低疾病严重程度、炎症细胞浸润、继发性脱髓鞘和轴突丢失，从而减少神经死亡。总之，我们的研究表明，通过改善炎症环境，这种联合治疗可能为 NMO 动物模型提供一种缓解进行性失明和瘫痪的治疗方法。
