Department of Nursing, CLINURSID Research group, School of Nursing, University of Santiago de Compostela, Santiago de Compostela, Spain; Department of Anesthesiology, Critical Care and Pain Management, Critical Patient Translational Research Group, Hospital Clínico Universitario, Health Research Institute of Santiago de Compostela (IDIS), University of Santiago de Compostela, Santiago de Compostela, Spain.
Department of Neurology, Clinical Neurosciences Research Laboratory, Hospital Clínico Universitario, Health Research Institute of Santiago de Compostela (IDIS), University of Santiago de Compostela, Santiago de Compostela, Spain.
Life Sci. 2016 Jan 1;144:162-9. doi: 10.1016/j.lfs.2015.12.007. Epub 2015 Dec 3.
Dexmedetomidine is a selective agonist of α2-adrenergic receptors with clinical anesthetic and analgesic properties that has also shown neuroprotective effects on several models of brain injury. Because perioperative stroke and brain damage are frequent causes of death in critical care units, we aimed to investigate neuroprotective properties of dexmedetomidine using an in vitro model of cerebral ischemia.
Primary mixed rat brain cortical cultures were subjected to oxygen and glucose deprivation and treated with different doses of dexmedetomidine in order to analyze three conditioning strategies: preconditioning, intraconditioning and postconditioning.
All dexmedetomidine pre-, intra- and postconditioning treatments showed neuroprotective effects reducing brain cell necrosis, although only preconditioning showed antiapoptotic effects. Dexmedetomidine treatments also reduced IL-6 and TNF-α levels, especially in the preconditioning groups. Oxidative stress was attenuated with all dexmedetomidine preconditioning treatments, but only with the higher dose in the intraconditioning group, and no effects were observed in the postconditioning. All conditioning strategies increased BDNF levels.
Dexmedetomidine-mediated neuroprotective effects in an in vitro model of cerebral ischemia involve the attenuation of inflammation and oxidative stress and the increment of BDNF expression.
右美托咪定是一种选择性α2-肾上腺素能受体激动剂,具有临床麻醉和镇痛作用,已在多种脑损伤模型中显示出神经保护作用。由于围手术期卒中与脑损伤是重症监护病房中常见的死亡原因,我们旨在通过体外脑缺血模型来研究右美托咪定的神经保护特性。
原代混合大鼠皮质培养物经历氧和葡萄糖剥夺,并使用不同剂量的右美托咪定进行处理,以分析三种预处理策略:预处理、内预处理和后预处理。
所有右美托咪定预处理、内预处理和后预处理均表现出神经保护作用,可减少脑细胞坏死,尽管只有预处理显示出抗凋亡作用。右美托咪定处理还降低了 IL-6 和 TNF-α 水平,尤其是在预处理组中。所有右美托咪定预处理均减轻了氧化应激,但仅在内预处理组中高剂量时才观察到,在后预处理中则没有观察到。所有预处理策略均增加了 BDNF 水平。
右美托咪定在体外脑缺血模型中发挥的神经保护作用涉及炎症和氧化应激的减轻以及 BDNF 表达的增加。