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<p>Radiation-induced brain injury is caused by repeated radiation therapy for brain tumors and leukemia. Effective treatments for radiation-induced brain injury have not been developed. This study aimed to investigate the neuroprotective effects of umbilical cord-derived mesenchymal stromal cells (UC-MSCs) on irradiated neurons. We irradiated fetal mouse cortical neurons followed by coculture with UC-MSCs in vitro. Radiation significantly reduced the number of MAP2-positive mature and GAP43-positive immature neurons with a shortened neurite length, whereas coculture with UC-MSCs significantly restored the number and length of both MAP2-positive and GAP43-positive neurons. Irradiation induced apoptosis/necrosis in neurons significantly, while UC-MSCs prevented the neurons from apoptosis to necrosis. The incidence of reactive oxygen species (ROS) increased significantly in irradiated neurons compared to the control group, whereas it was significantly attenuated by the coculture of UC-MSCs. In conclusion, these results suggest that UC-MSCs have potential neuroprotective effects against radiation-induced brain injury by reducing oxidative stress.</p>

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Umbilical cord-derived mesenchymal stromal cells attenuate radiation-induced neuron damage in vitro

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月22日

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  • Trang Thi Binh Pham,
  • Kenshi Sei,
  • Yuki Yamamoto,
  • Takeo Mukai,
  • Hiroyuki Akai,
  • Tokiko Nagamura-Inoue

摘要

Radiation-induced brain injury is caused by repeated radiation therapy for brain tumors and leukemia. Effective treatments for radiation-induced brain injury have not been developed. This study aimed to investigate the neuroprotective effects of umbilical cord-derived mesenchymal stromal cells (UC-MSCs) on irradiated neurons. We irradiated fetal mouse cortical neurons followed by coculture with UC-MSCs in vitro. Radiation significantly reduced the number of MAP2-positive mature and GAP43-positive immature neurons with a shortened neurite length, whereas coculture with UC-MSCs significantly restored the number and length of both MAP2-positive and GAP43-positive neurons. Irradiation induced apoptosis/necrosis in neurons significantly, while UC-MSCs prevented the neurons from apoptosis to necrosis. The incidence of reactive oxygen species (ROS) increased significantly in irradiated neurons compared to the control group, whereas it was significantly attenuated by the coculture of UC-MSCs. In conclusion, these results suggest that UC-MSCs have potential neuroprotective effects against radiation-induced brain injury by reducing oxidative stress.