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Objective: Paraplegia is a dangerous complication of thoracoabdominal aortic surgery. Various studies have been conducted on the prevention of this complication and some spinal cord protection methods have been proposed. However, there is not any modality that prevent the development of paraplegia certainly. In the I / R period, primary injury triggers secondary injury due to increased inflammation, apoptosis and free radical formation. In this study, we evaluated that the neuroprotective effect of adalimumab in spinal cord ischemia-reperfusion injury.
Materials and Methods: In total, 24 adult New Zealand rabbits were divided into three groups: Group 1, control; Group 2, ischemia-reperfusion by infrarenal aortic clamping; Group 3, adalimumab treated followed by ischemia. Tissue and plasma tumor necrosis factor alpha, interleukin 6, interleukin 10, thiobarbituric acid reactive substance, total oxidant status and total antioxidant status levels were analyzed as a marker of inflammation and oxidation. Histopathological evaluation of the tissues was performed, and apoptosis was evaluated by TUNNEL method.
Results: I/R injury significantly increases plasma and spinal cord tissue at TNF alpha, TOS, TBARS, IL6 levels and reduces plasma and spinal cord tissue to TAS and IL10 levels. Adalimumab treatment significantly reduces plasma and spinal cord tissue to TNF alpha, TOS, TBARS, IL6 and increases plasma and tissue to TAS and IL10 levels.
Conclusion: Adalimumab treatment significantly reduces the spinal cord neuronal damage score and the number of apoptotic cells. This paper aims to demonstrate the important neuroprotective effects of adalimumab on rabbit spinal cord I/R injury.