Therapeutic effect and mechanism of hUC-MSCs in experimental autoimmune encephalomyelitis mice

HUANG Ying; JIN Zi-yi; HAO Xiao-fang; HOU Tian-tian; QIN Chao; ZHANG Yi-kun; GENG Xing-chao

doi:10.20251/j.cnki.1003-3734.2025.20.007

Abstract：Objective:To investigate the therapeutic effect and potential mechanism of human umbilical cord mesenchymal stem cells(hUC-MSC)on experimental autoimmune encephalomyelitis mouse model,and provide experimental basis for the treatment of multiple sclerosis with hUC-MSC.Methods:A model was constructed in C57BL/6J female mice induced by myelin oligodendrocyte glycoprotein and pertussis toxin,followed by a single tail vein injection of hUC-MSC(1×106 cells per mouse)for in vivo treatment.The neurological function score changes of mice with experimental autoimmune encephalomyelitis after hUC-MSC therapy was observed,the improvement of spinal cord demyelinating lesions was evaluated,and cytokine screening was conducted to further explore the mechanism of hUC-MSC in regulating immune response and promoting nerve repair.For in vitro validation,human umbilical cord mesenchymal stem cells were co-cultured with oligodendrocyte precursor cells to detect the proliferation indexes and differentiated cell morphology of mouse oligodendrocyte precursor cells,so as to study the regulatory effect of hUC-MSC on mouse oligodendrocyte precursor cells and provide data support for clinical application.Results:In vivo experiments showed that hUC-MSC could significantly improve neurological dysfunction,reduce neurological function scores,and reduce spinal cord demyelination and inflammatory cell infiltration in mice with experimental autoimmune encephalomyelitis.In vitro validation showed that hUC-MSC significantly promoted the proliferation and differentiation of mouse oligodendrocyte precursor cells.Conclusion:hUC-MSC have a significant therapeutic effect on mice with experimental autoimmune encephalomyelitis,and the mechanism may be related to regulation of immune response,promotion of nerve repair,and regulation of the proliferation and differentiation of oligodendrocyte precursor cells.