主管单位:中华人民共和国
国家卫生健康委员会
主办单位:
总编辑:杨秋
编辑部主任:吴翔宇
邮发代号:80-528
定价:28.00元
全年:336.00元
Email:zgyy8888@163.com
电话(传真):010-64428528;
010-64456116(总编室)
英文单位:Department of Anesthesiology the Affiliated Hospital of Guizhou Medical University Guiyang 550004 China
英文关键词:Dexmedetomidine;Neuroprotection;Apoptosis;Pyroptosis
右美托咪定作为一种高选择性α2肾上腺素受体激动剂,具有镇痛、镇静、稳定脑血流和防治术后谵妄等作用。对于神经系统而言,已有研究证实它的神经保护作用是通过抗炎、抑制细胞凋亡、减少儿茶酚胺释放、抑制兴奋性神经毒性等多信号通路共同参与完成。近年来,对于右美托咪定还可能通过减轻细胞焦亡来发挥神经保护效应这一研究已成为热点,但是其具体分子机制和信号通路仍未完全阐明。本文对右美托咪定调控中枢神经细胞凋亡和细胞焦亡发挥神经保护作用的机制进行综述。
Dexmedetomidine, as a highly selective α2 adrenergic receptor agonist, has effect on analgesia, sedative, stablilizing cerebral blood flow, and prevention and treatment of postoperative delirium. For the nervous system, studies have confirmed its nerve protective effect through anti-inflammatory, inhibiting cell apoptosis, reducing catecholamine release and inhibiting excitatory neurotoxicity signaling pathways in together. In recent years, the research that dexmedetomidine may also exert neuroprotective effect by reducing pyroptosis has become a hot spot. However, the specific molecular mechanism and signaling pathway are still not fully elucidated. This article reviews the mechanism of neuroprotective effects of dexmedetomidine on central nerve cell apoptosis and pyroptosis.
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