右美托咪定抗缺血再灌注损伤作用机制的研究现状  

Mechanism of dexmedetomidine against ischemia reperfusion injury

作　　者：刘振臻 李轩杰 冷玉芳[1,2] 张广儒 刘迪生 赵志宇 薛兴[2] Liu Zhen-zhen;Li Xuan-jie;Leng Yu-fang;Zhang Guang-ru;Liu Di-sheng;Zhao Zhi-yu;Xue Xing(The First School of Clinical Medicine,Lanzhou University,Lanzhou 730000,China;Department of Anesthesiology,The First Hospital of Lanzhou University,Lanzhou 730000,China)

机构地区：[1]兰州大学第一临床医学院,甘肃兰州730000 [2]兰州大学第一医院麻醉科,甘肃兰州730000

出　　处：《兰州大学学报（医学版）》2020年第4期1-5,共5页Journal of Lanzhou University（Medical Sciences）

基　　金：甘肃卫生行业科研计划项目(GSWSKY2017-18);国家自然科学基金资助项目(81960345)。

摘　　要：缺血再灌注损伤围手术期发生率和死亡率极高。右美托咪定是一种选择性α2肾上腺素能受体激动剂,广泛应用于临床麻醉和重症监护病房镇静。右美托咪定对缺血再灌注损伤有保护作用,它通过清除自由基、抗氧化、减轻氧化应激反应损伤,通过抑制TLR4/NF-κB通路减轻炎症反应,通过线粒体途径和PI3K/Akt信号通路抗细胞凋亡,通过Bcl-2/Beclin-1信号通路和上调HIF-1α等抗自噬,减轻缺血再灌注损伤。The perioperative incidence and mortality of ischemia reperfusion(IR) injury are extremely high.Dexmedetomidine(Dex), a selective 2 adrenergic receptor agonist, is widely used in clinical anesthesia and intensive care unit sedation. It was shown that dexmedetomidine has a protective effect on IR injury, it can reduce oxidative stress injury by scavenging free radicals, inhibiting the TLR4/NF-κB pathway, alleviating inflammatory reaction, preventing apoptosis by mitochondrial and PI3K/Akt signaling pathways, preventing autophagy by the Bcl-2/Beclin-1 signaling pathway and upregulating HIF-1α to alleviate IR injury.

关 键 词：右美托咪定 缺血再灌注损伤 抗炎 抗凋亡 抗自噬 

分 类 号：R619[医药卫生—外科学]