Dexmedetomidine attenuates spinal cord ischemia-reperfusion injury through both anti-inflammation and anti-apoptosis mechanisms in rabbits

Journal of Translational Medicine
Zhixiang SunHao Weng

Abstract

Dexmedetomidine (Dex) can improve neuronal viability and protect the spinal cord from ischemia-reperfusion (I/R) injury, but the underlying mechanisms are not fully understood. This study investigated the effects of dexmedetomidine on the toll-like receptor 4 (TLR4)-mediated nuclear factor κB (NF-κB) inflammatory system and caspase-3 dependent apoptosis induced by spinal cord ischemia-reperfusion injury. Twenty-four rabbits were divided into three groups: I/R, Dex (10 µg/kg/h prior to ischemia until reperfusion), and Sham. Abdominal aortic occlusion was carried out for 30 min in the I/R and Dex groups. Hindlimb motor function was assessed using the Tarlov scoring system for gait evaluation. Motor neuron survival and apoptosis in the ventral grey matter were assessed by haematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labelling staining. The expression and localisation of ionised calcium-binding adaptor molecule 1, TLR4, NF-κB and caspase-3 were assessed by immunoreactivity analysis. The levels of interleukin 1β and tumour necrosis factor α were assessed using enzyme-linked immunosorbent assays. Perioperative treatment with dexmedetomidine was associated with a significant prese...Continue Reading

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Citations

Sep 5, 2019·The Kaohsiung Journal of Medical Sciences·Jian HaoQun-Sheng Hu
Apr 1, 2020·The Journal of Spinal Cord Medicine·Kevser TuralIrfan Tasoglu
Aug 28, 2020·Journal of Clinical Medicine·Mohamed MahmoudKeira P Mason
Jun 23, 2021·Journal of Cardiothoracic and Vascular Anesthesia·Mina OftadehMichael Haske
Apr 27, 2020·Experimental and Molecular Pathology·Xiao-Ming LiuXue-Kang Zhang

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis