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.
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.
Authors: Dae Young Yoo; Dae Won Kim; Jin Young Chung; Hyo Young Jung; Jong Whi Kim; Yeo Sung Yoon; In Koo Hwang; Jung Hoon Choi; Goang-Min Choi; Soo Young Choi; Seung Myung Moon Journal: Neurochem Res Date: 2016-10-14 Impact factor: 3.996
Authors: C H Hulme; S J Brown; H R Fuller; J Riddell; A Osman; J Chowdhury; N Kumar; W E Johnson; K T Wright Journal: Spinal Cord Date: 2016-12-20 Impact factor: 2.772
Authors: Ergün Karavelioğlu; Yücel Gönül; Serdar Kokulu; Ömer Hazman; Fatih Bozkurt; Ahmet Koçak; Olcay Eser Journal: Inflammation Date: 2014-06 Impact factor: 4.092