Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (12): 2702-2709.doi: 10.4103/1673-5374.339491

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Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis

Yi-Xin Chen1, 2, 3, 4, 5, 6, Talifu Zuliyaer1, 2, 3, 4, 5, Bin Liu7, Shuang Guo1, 2, 3, 4, 5, De-Gang Yang1, 2, 3, 4, 5, Feng Gao1, 2, 3, 4, 5, *, Yan Yu2, 3, 5, Ming-Liang Yang1, 2, 3, 4, 5, Liang-Jie Du1, 2, 3, 4, 5, Jian-Jun Li1, 2, 3, 4, 5, *#br#   

  1. 1School of Rehabilitation Medicine, Capital Medical University, Beijing, China; 2China Rehabilitation Science Institute, Beijing, China; 3Center of Neural Injury and Repair, Beijing Institute for Brain Disorders, Beijing, China; 4Department of Spinal and Neural Functional Reconstruction, China Rehabilitation Research Center, Beijing, China; 5Beijing Key Laboratory of Neural Injury and Rehabilitation, Beijing, China; 6Department of Rehabilitation Medicine, Xiangya Hospital of Central South University, Changsha, Hunan Province, China; 7Department of Spine Surgery, Hunan Provincial People’s Hospital (The First Affiliated Hospital of Hunan Normal University), Changsha, Hunan Province, China
  • Online:2022-12-15 Published:2022-05-05
  • Contact: Jian-Jun Li, 13718331416@163.com; Feng Gao, PhD, gaofeng5960@126.com.
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 81870979 (to JJL); the Scientific Research Foundation of China Rehabilitation Research Center, No. 2020-02 (to JJL); and the Natural Science Foundation of Changsha, No. kq2014285 (to YXC).

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Abstract: Ferroptosis is a recently discovered form of iron-dependent cell death, which occurs during the pathological process of various central nervous system diseases or injuries, including secondary spinal cord injury. Selenium has been shown to promote neurological function recovery after cerebral hemorrhage by inhibiting ferroptosis. However, whether selenium can promote neurological function recovery after spinal cord injury as well as the underlying mechanism remain poorly understood. In this study, we injected sodium selenite (3 µL, 2.5 µM) into the injury site of a rat model of T10 vertebral contusion injury 10 minutes after spinal cord injury modeling. We found that sodium selenite treatment greatly decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal. Furthermore, sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4, promoted the survival of neurons and oligodendrocytes, inhibited the proliferation of astrocytes, and promoted the recovery of locomotive function of rats with spinal cord injury. These findings suggest that sodium selenite can improve the locomotive function of rats with spinal cord injury possibly through the inhibition of ferroptosis via the specificity protein 1/glutathione peroxidase 4 pathway. 

Key words: ferroptosis, glutathione peroxidase 4, glutathione, iron, lipid peroxidation, neural regeneration, secondary injury, sodium selenite, specificity protein 1, spinal cord injury