Conclusions
The elevated M2 macrophages ameliorated the clinical severity of EAN by
downregulating the activation of NF-κB p65 and the accumulation of
pro-inflammatory M1 macrophages and cytokines. Furthermore, BAY11-7082
as a inhibitor of NF-κB attenuated EAN through mediating the phenotypic
shift in macrophages from M1 to M2 cells. The anti-inflammatory effects
of BAY11-7082 on EAN are probably restoring the balance of M1-M2
macrophages and their cytokines. NF-κB inhibitor may be a potent
candidate for the treatment of poly-neuritic diseases in the future.