右美托咪定神经保护机制的研究进展

Research Progress on the Neuroprotective Mechanisms of Dexmedetomidine

长时间接受全身麻醉会损害发育期认知功能的形成,也会加速老年认知功能退化。近年来研究发现,右美托咪定(Dex)作为一种α2肾上腺素能受体激动剂,不仅能与其他麻醉药联合使用,从而减少其他全身麻醉药的用量,还可以减轻麻醉药诱发的神经细胞氧化应激、细胞凋亡和线粒体损伤等,起到一定的神经保护作用。因此,本文从神经炎症和炎性因子释放、氧化应激、基因表达、细胞自噬、细胞凋亡、突触可塑性和神经发生等角度系统阐述Dex在麻醉过程中神经保护的作用机制,为进一步研究Dex的神经保护机理提供理论依据,为其在兽医临床和比较医学领域中的进一步应用提供参考。

Prolonged exposure to general anesthesia can impair the formation of cognitive function during the developmental period and accelerate age-related cognitive decline.In recent years,it has been found that dexmedetomidine(Dex),as anα2-adrenergic receptor agonist,not only reduces the dosage of other general anesthetics when used in combination,but also alleviates anesthesia-induced neuronal oxidative stress,cell apoptosis,and mitochondrial damage,thus exerting a certain neuroprotective effect.Therefore,this article systematically elucidates the neuroprotective mechanisms of Dex during anesthesia from the perspectives of neuroinflammation and release of inflammatory cytokine,oxidative stress,gene expression,cellular autophagy,cell apoptosis,synaptic plasticity,and neurogenesis.It provides a theoretical basis for further exploring the neuroprotective mechanisms of Dex and serves as a reference for its future application in veterinary clinical and comparative medicine.