Guillain–Barré syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of the peripheral nervous system (PNS). Macrophages play a central role in its animal model, experimental autoimmune neuritis (EAN), which has been well accepted. Additionally, nuclear factor (NF)-κB inhibitors have been used to treat cancers and have shown beneficial effects. Here, we investigated the therapeutic effect of M2 macrophage and the NF-κB pathway’s correlation with macrophage activation in EAN in C57BL/6 mice. We demonstrate that M2 macrophage transfusion could alleviate the clinical symptoms of EAN by reducing the proportion of M1 macrophage in the peak period, inhibiting the phosphorylation of NF-κB p65. The NF-κB inhibitor (BAY-11-7082) could alleviate the clinical symptoms of EAN and shorten the duration of symptoms by reducing the proportion of M1 macrophages and the expression of proinflammatory cytokines. Consequently, BAY-11-7082 exhibits strong potential as a therapeutic strategy for ameliorating EAN by influencing the balance of M1/M2 macrophages and inflammatory cytokines.

中文翻译：

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核因子 kappa B 抑制剂通过降低巨噬细胞极化至 M1 型来抑制小鼠实验性自身免疫性神经炎

格林-巴利综合征 (GBS) 是一种急性炎症和免疫介导的周围神经系统 (PNS) 脱髓鞘疾病。巨噬细胞在其动物模型实验性自身免疫性神经炎 (EAN) 中发挥核心作用，该模型已被广泛接受。此外，核因子 (NF)-κB 抑制剂已被用于治疗癌症并显示出有益效果。在这里，我们研究了 M2 巨噬细胞的治疗效果以及 NF-κB 通路与 C57BL/6 小鼠 EAN 中巨噬细胞活化的相关性。我们证明M2巨噬细胞输注可以通过降低高峰期M1巨噬细胞的比例，抑制NF-κB p65的磷酸化来缓解EAN的临床症状。NF-κB抑制剂（BAY-11-7082）可通过降低M1巨噬细胞比例和促炎细胞因子的表达来缓解EAN的临床症状并缩短症状持续时间。因此，BAY-11-7082 显示出作为通过影响 M1/M2 巨噬细胞和炎性细胞因子的平衡来改善 EAN 的治疗策略的强大潜力。