The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury

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 c...

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Main Authors: Yasar Karatas, Mehmet Fatih Erdi, Bulent Kaya, Fatih Keskin, İbrahim Kılınç, Mehmet Uyar, Sabiha Serpil Kalkan, Emir Kaan Izci, Erdal Kalkan
Format: Article
Language:English
Published: London Academic Publishing 2020-06-01
Series:Romanian Neurosurgery
Subjects:
Online Access:https://www.journals.lapub.co.uk/index.php/roneurosurgery/article/view/1504
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author Yasar Karatas
Mehmet Fatih Erdi
Bulent Kaya
Fatih Keskin
İbrahim Kılınç
Mehmet Uyar
Sabiha Serpil Kalkan
Emir Kaan Izci
Erdal Kalkan
author_facet Yasar Karatas
Mehmet Fatih Erdi
Bulent Kaya
Fatih Keskin
İbrahim Kılınç
Mehmet Uyar
Sabiha Serpil Kalkan
Emir Kaan Izci
Erdal Kalkan
author_sort Yasar Karatas
collection DOAJ
description 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.
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spelling doaj.art-a4895fc7bd1f4db2b2deb6a3ffa5a8a92022-12-22T00:57:39ZengLondon Academic PublishingRomanian Neurosurgery1220-88412344-49592020-06-0134210.33962/roneuro-2020-056The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injuryYasar KaratasMehmet Fatih ErdiBulent KayaFatih Keskinİbrahim KılınçMehmet UyarSabiha Serpil KalkanEmir Kaan IzciErdal KalkanObjective: 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.https://www.journals.lapub.co.uk/index.php/roneurosurgery/article/view/1504spinalischemia-reperfusionneuroprotectioninflammationadalimumab
spellingShingle Yasar Karatas
Mehmet Fatih Erdi
Bulent Kaya
Fatih Keskin
İbrahim Kılınç
Mehmet Uyar
Sabiha Serpil Kalkan
Emir Kaan Izci
Erdal Kalkan
The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
Romanian Neurosurgery
spinal
ischemia-reperfusion
neuroprotection
inflammation
adalimumab
title The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
title_full The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
title_fullStr The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
title_full_unstemmed The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
title_short The efficacy of adalimumab on experimentally induced spinal cord ischemia-reperfusion injury
title_sort efficacy of adalimumab on experimentally induced spinal cord ischemia reperfusion injury
topic spinal
ischemia-reperfusion
neuroprotection
inflammation
adalimumab
url https://www.journals.lapub.co.uk/index.php/roneurosurgery/article/view/1504
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