Background <p>Human umbilical cord mesenchymal stem cells (hUC-MSCs) have great potential for treating autoimmune diseases for their immunomodulatory and tissue-regenerative abilities; however, their therapeutic role in neuromyelitis optica spectrum disorder (NMOSD) remains uncertain.</p> Methods <p>10<sup>6</sup> hUC-MSCs prepared in 200&#xa0;μl PBS were intravenously administered to a systemic NMOSD model on day 10 and day 14 after immunization. Then, disease progression, immune responses, and blood–brain barrier integrity were evaluated. Additionally, we tested the effects of hUC-MSCs on astrocyte viability and apoptosis using an aquaporin 4 (AQP4) IgG and complement-induced cytotoxicity model in vitro.</p> Results <p>hUC-MSCs alleviated NMOSD progression in vivo with improved motor function, reduced inflammatory infiltration, myelin loss, and preservation of astrocytes and neurons. hUC-MSC treatment did not affect autoimmune reactions in the spleen, however, decreased cytokine release in the spinal cord and mitigated blood–brain barrier disruption. Furthermore, in vitro studies revealed that co-culture with hUC-MSCs significantly restored astrocyte viability and reduced apoptosis in AQP4 IgG and complement-mediated damage.</p> Conclusion <p>Our results revealed that hUC-MSCs displayed therapeutic efficacy in NMOSD and showed potential in attenuating blood–brain barrier disruption, as well as AQP4 IgG and complement-induced astrocyte apoptosis.</p>

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Efficacy of human umbilical cord mesenchymal stem cell in the treatment of neuromyelitis optica spectrum disorders: an animal study

  • Chunran Xue,
  • Haojun Yu,
  • Xuzhong Pei,
  • Xiaoying Yao,
  • Jie Ding,
  • Xiying Wang,
  • Yi Chen,
  • Yangtai Guan

摘要

Background

Human umbilical cord mesenchymal stem cells (hUC-MSCs) have great potential for treating autoimmune diseases for their immunomodulatory and tissue-regenerative abilities; however, their therapeutic role in neuromyelitis optica spectrum disorder (NMOSD) remains uncertain.

Methods

106 hUC-MSCs prepared in 200 μl PBS were intravenously administered to a systemic NMOSD model on day 10 and day 14 after immunization. Then, disease progression, immune responses, and blood–brain barrier integrity were evaluated. Additionally, we tested the effects of hUC-MSCs on astrocyte viability and apoptosis using an aquaporin 4 (AQP4) IgG and complement-induced cytotoxicity model in vitro.

Results

hUC-MSCs alleviated NMOSD progression in vivo with improved motor function, reduced inflammatory infiltration, myelin loss, and preservation of astrocytes and neurons. hUC-MSC treatment did not affect autoimmune reactions in the spleen, however, decreased cytokine release in the spinal cord and mitigated blood–brain barrier disruption. Furthermore, in vitro studies revealed that co-culture with hUC-MSCs significantly restored astrocyte viability and reduced apoptosis in AQP4 IgG and complement-mediated damage.

Conclusion

Our results revealed that hUC-MSCs displayed therapeutic efficacy in NMOSD and showed potential in attenuating blood–brain barrier disruption, as well as AQP4 IgG and complement-induced astrocyte apoptosis.