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

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

Neural Regeneration Research, 2022 · DOI: https://doi.org/10.4103/1673-5374.339491 · Published: December 1, 2022

Spinal Cord InjuryRegenerative MedicineGenetics

Simple Explanation

Spinal cord injury (SCI) can lead to secondary damage, including a type of cell death called ferroptosis. This process involves iron buildup and toxic lipid production. The study explores whether sodium selenite, a selenium compound, can aid recovery after SCI by preventing ferroptosis. The researchers found that sodium selenite treatment reduced iron levels and harmful lipid byproducts in rats with spinal cord injuries. It also boosted levels of proteins that protect cells and helped nerve cells survive. The study suggests that sodium selenite may improve recovery from spinal cord injuries by preventing ferroptosis through a specific molecular pathway involving proteins called specificity protein 1 (SP1) and glutathione peroxidase 4 (GPX4).

Study Duration
8 weeks
Participants
Wistar rats (n = 35 per group for formal study)
Evidence Level
Not specified

Key Findings

  • 1
    Sodium selenite treatment decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal in a rat model of spinal cord injury.
  • 2
    Sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4.
  • 3
    Sodium selenite 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.

Research Summary

This study investigated the potential of sodium selenite (SS) to promote neurological function recovery after spinal cord injury (SCI) by inhibiting ferroptosis in a rat model. The results showed that SS treatment decreased iron concentration and lipid peroxidation, increased the expression of specificity protein 1 (SP1) and glutathione peroxidase 4 (GPX4), and promoted the survival of neurons and oligodendrocytes. The findings suggest that SS can improve locomotive function in rats with SCI, possibly through the inhibition of ferroptosis via the SP1/GPX4 pathway.

Practical Implications

Therapeutic Potential

Sodium selenite may represent a promising therapeutic agent for mitigating secondary damage and promoting neurological recovery following spinal cord injury.

Targeted Intervention

The identification of the SP1/GPX4 pathway as a key mechanism suggests a target for developing more specific and effective treatments for SCI.

Further Research

Additional studies are warranted to explore the optimal dosage, timing, and delivery methods of sodium selenite, as well as to validate these findings in clinical trials.

Study Limitations

  • 1
    Short experimental time limits long-term effects analysis.
  • 2
    Lack of direct binding relationships and exact mechanisms for the selenium/SP1/GPX4 axis.
  • 3
    Small sample size limits the statistical power of the results.

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