Guillain–Barre’ syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of peripheral nervous system (PNS). Macrophages playing a central role in its animal model, experimental autoimmune neuritis (EAN) has been well-accepted. Additionally, NF-κB inhibitors has been used to treat cancers and showed beneficial effects. Here we investigated the therapeutic effect of M2 macrophage and NF-κB pathway is correlated with macrophages activation in experimental autoimmune neuritis (EAN) in C57BL/6 mice. We demonstrated that M2 macrophage transfusion can 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 pro-inflammatory 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.