Analysis of serum pro-inflammatory cytokine levels after rat spinal cord ischemia/reperfusion injury and correlation with tissue damage

Turk Neurosurg. 2009 Oct;19(4):353-9.

Abstract

Aim: A rat model of spinal cord ischemia/reperfusion was conducted and the serum cytokine levels and histopathological changes were assessed.

Material and methods: Twenty-four male Sprague-Dawley rats were assigned into four experimental groups. Group-A (the sham operated rats) and group-B (the spinal ischemia/reperfusion group) were sacrificed at 24 hours postoperatively while group-C (the sham operated rats) and group-D (the spinal ischemia/reperfusion group) were sacrificed at 48 hours. Histopathological changes in the spinal cords and serum cytokine levels were analysed.

Results: All three proinflammatory cytokine levels reached significantly higher levels compared to the sham operated groups in both the 24-hour and 48-hour spinal cord ischemia/reperfusion groups.

Conclusion: Inflammation is a plausible pathway in spinal cord ishemia/reperfusion injury. However clinical treatment of the damage does not currently include antiinflammatory therapy. The results of our study supported the hypothesis that inflammatory responses could play a possible role in the ischemia/reperfusion injury of the spinal cord. Characterization of the role of inflammation in the etiopathogenesis of ischemia/reperfusion injury to the spinal cord is important to facilitate the development of novel therapeutic approaches for prevention and/or treatment of this severe condition.

MeSH terms

  • Animals
  • Biomarkers / blood
  • Cytokines / blood*
  • Disease Models, Animal
  • Interleukin-1beta / blood
  • Interleukin-6 / blood
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / immunology*
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / pathology
  • Spinal Cord Diseases / immunology*
  • Spinal Cord Diseases / metabolism*
  • Spinal Cord Diseases / pathology
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Biomarkers
  • Cytokines
  • Interleukin-1beta
  • Interleukin-6
  • Tumor Necrosis Factor-alpha