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  4. Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

Electroacupuncture Treatment Suppresses Transcription Factor IRF8 in Spinal Cord of Rats with Spared Nerve Injury

Pain Research and Management, 2020 · DOI: https://doi.org/10.1155/2020/1854363 · Published: April 10, 2020

Alternative MedicinePain ManagementGenetics

Simple Explanation

Neuropathic pain is a major health problem, and new treatments are needed. Electro-acupuncture (EA) can help with neuropathic pain after nerve injury, but how it works is not fully understood. This study looks at whether EA can reduce Interferon Regulatory Factor 8 (IRF8) in the spinal cords of rats with nerve injury. The study involved electro-acupuncture treatment of rats with spared nerve injury (SNI). The treatment was administered every other day for 21 days. Paw withdrawal threshold (PWT) was measured to assess pain. Spinal IRF8 and CX3CRl expressions were detected. The study found that nerve injury increased IRF8 and CX3CRl expression. EA treatment reduced IRF8 and CX3CRl expression, and also reduced sensitivity to pain. This suggests that EA works by targeting IRF8 and reducing inflammation in the spinal cord.

Study Duration
21 days
Participants
Sprague Dawley rats (weighing 160–180 g)
Evidence Level
Not specified

Key Findings

  • 1
    Spared nerve injury (SNI) significantly increased spinal IRF8 and CX3CRl mRNA and protein expression in rats.
  • 2
    2 Hz electroacupuncture (EA) treatment of SNI rats reduced IRF8 and CX3CRl mRNA and protein expression in the spinal cord.
  • 3
    2 Hz EA treatment reversed the coexpression of IRF8 or CX3CRl with CD11b (a microglial activation marker) in the spinal cord of SNI rats.

Research Summary

This study investigates the effect of 2 Hz electroacupuncture (EA) on neuropathic pain in rats with spared nerve injury (SNI), focusing on the role of interferon regulatory factor 8 (IRF8) and CX3CRl in the spinal cord. The results show that SNI induces significant elevation of spinal IRF8 and CX3CRl mRNA and protein expression, along with coexpression of IRF8 and CX3CRl with the microglial activation marker CD11b. 2 Hz EA treatment attenuates SNI-evoked mechanical hypersensitivity and reverses the increase in IRF8 and CX3CRl expression, suggesting that targeting IRF8 may be a promising therapeutic strategy for neuropathic pain.

Practical Implications

Therapeutic Target

Targeting IRF8 may be a promising therapeutic strategy for 2 Hz EA treatment of neuropathic pain.

Mechanism Elucidation

Provides further insight into the mechanisms underlying 2 Hz EA in treating SNI-evoked neuropathic pain.

Alternative Treatment

2 Hz EA can effectively alleviate mechanical hypersensitivity in SNI rats.

Study Limitations

  • 1
    The correlation of IRF8 or CX3CRl with microglial activation in the spinal cord following SNI by 2 Hz EA with inhibitors needs further definition.
  • 2
    Further studies are needed to define the correlation of IRF8 or CX3CRl with microglial activation.
  • 3
    Not specified

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