Multiple sclerosis (MS), a disease in which the immune system attacks nerve cells, has been associated with both genetic and environmental risk factors. We observed increased micronucleus (MN) formation in SJL/J mouse experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Most of these MN were due to chromosomal loss. Increased activation of MAP kinases, which leads to disruption of the mitotic spindle and improper segregation of chromosomes, is associated with MS. MAP kinase inhibitors, such as PD98059, may therefore be beneficial for MS. In the EAE model, PD98059 treatment reduced adverse effects, including MN formation, lipid peroxidation, and GSH oxidation. Interventions that mitigate chromosomal instability may have therapeutic value in MS.

多发性硬化症 (MS) 是一种免疫系统攻击神经细胞的疾病，与遗传和环境风险因素有关。我们观察到 SJL/J 小鼠实验性自身免疫性脑脊髓炎 (EAE)（一种 MS 动物模型）中微核 (MN) 形成增加。大多数这些 MN 是由于染色体丢失。MAP 激酶激活的增加会导致有丝分裂纺锤体的破坏和染色体的不当分离，这与 MS 相关。因此，MAP 激酶抑制剂，例如 PD98059，可能对 MS 有益。在 EAE 模型中，PD98059 治疗减少了不良反应，包括 MN 形成、脂质过氧化和 GSH 氧化。减轻染色体不稳定性的干预措施可能对 MS 具有治疗价值。