PubMed · 2009 · 73 citations · 30 references
Veterinary MedicineImmunologyPathobiologyImmunopathologyInflammationNeuroimmunologyAcute InflammationCytokine BiologyInflammatory PathologyInflammatory Tissue InjuryNeuroinflammationSpinal Cord InjuryInflammatory Tissue DamageIschemic Injury ResponseNeuroinflammatory CytokinesPro-inflammatory Cytokine CascadesPro-inflammatory Cytokine ExpressionSpinal Cord InfarctionTissue Damage MechanismsTissue Damage Response
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.
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