摘要
背景:右旋美托咪定具有抗缺血再灌注损伤的作用,但对其信号通路全面、系统的综述较少。目的:重点对右旋美托咪定在抗氧化应激、抑制炎症、抗凋亡、自噬等机制方面的信号通路进行综述。方法:计算机检索PubMed数据库、中国知网、万方数据库及维普数据库的相关文章,英文检索词为“ischemia-reperfusion injury,dexmedetomidine,signal path,oxidative stress,inflammation,apoptosis”;中文检索词为“缺血再灌注损伤,右旋美托咪定,信号通路,氧化应激,炎症,凋亡”。排除重复性研究及部分相关性较低的基础类文章,最终纳入57篇文献进行评价。结果与结论:①右旋美托咪定主要通过抗氧化应激损伤、抗炎、抗细胞凋亡和自噬等多种机制发挥器官保护作用,这其中又涉及众多通路,主要包括Nrf2及其下游蛋白抗氧化应激通路、Toll样受体4家族和核因子κB相关抗炎通路、JAK2/STAT3相关抗炎通路、胆碱能抗炎通路,而且胆碱能通路是众多核因子κB信号通路的上游机制;②PI3K/Akt通路依据其激活的下游信号不同发挥不同的作用,抑制NLRP3炎性体激活,激活内皮型一氧化氮合酶、哺乳动物雷帕霉素靶蛋白、缺氧诱导因子1α等信号分子发挥抗炎作用,激活Bad或Bax残基发挥抗凋亡作用,PI3K/Akt激活糖原合成酶激酶3β可同时发挥抗炎、抗凋亡作用;③右旋美托咪定激活SIRT3介导抗细胞凋亡作用,抑制内质网应激产生抗凋亡作用;④针对右旋美托咪定抗缺血再灌注损伤信号通路的详细综述,能为将来的机制研究及诊疗决策提供依据。
BACKGROUND:Dexmedetomidine has the effect of anti-ischemia-reperfusion injury,but the comprehensive and systematic review of its signaling pathway is less.OBJECTIVE:To focus on the review of dexmedetomidine’s signaling pathway in the mechanisms of antioxidant stress,inhibition of inflammation,anti-apoptosis,autophagy,and so on.METHODS:The relevant articles on PubMed,CNKI,WanFang,and VIP databases were searched by computer with the key words“ischemia-reperfusion inquiry;dexmedetomidine;signal path;oxidative stress;inflammation;apoptosis”in Chinese and English.After excluding repetitive research and some basic articles with low correlation,57 articles were finally included for review.RESULTS AND CONCLUSION:(1)Dexmedetomidine plays an important role in organ protection through many mechanisms,such as anti-oxidative stress injury,anti-inflammation,anti-apoptosis and autophagy.This involves many pathways,including Nrf2 and its downstream protein antioxidant stress pathway,Toll-like receptor 4 family and nuclear factor-κB-related anti-inflammatory pathway,JAK2/STAT3-related anti-inflammatory pathway,and cholinergic anti-inflammatory pathway,and the cholinergic pathway is the upstream mechanism of many nuclear factor-κB signaling pathways.(2)PI3K/Akt pathway plays different roles according to its activated downstream signals,inhibiting the activation of NLRP3 inflammatory body,activating signal molecules endothelial nitric oxide synthase,mammalian target of rapamycin,and hypoxia-inducible factor 1αto play an anti-inflammatory role,and activate Bad or Bax residues to play an antiapoptotic role,and PI3K/Akt activates glycogen synthetase kinase-3β.It can also play an anti-inflammatory and anti-apoptotic role.(3)Dexmedetomidine activates SIRT3 to mediate anti-apoptosis and inhibit endoplasmic reticulum stress to produce anti-apoptosis.(4)The detailed review of the anti-ischemiareperfusion injury signaling pathway of dexmedetomidine can provide a basis for future mechanism research and diagnosis and treatment decisions.
作者
杨毅峰
叶楠
王琳
郭帅成
黄健
Yang Yifeng;Ye Nan;Wang Lin;Guo Shuaicheng;Huang Jian(Second Affiliated Hospital of Inner Mongolia Medical University,Hohhot 010000,Inner Mongolia Autonomous Region,China)
出处
《中国组织工程研究》
CAS
北大核心
2024年第9期1464-1469,共6页
Chinese Journal of Tissue Engineering Research
基金
内蒙古医科大学青年项目(YKD2022QN034),项目负责人:杨毅峰
2022年度内蒙古自治区卫生健康科技计划项目(202201352),项目负责人:黄健。
关键词
缺血再灌注损伤
右旋美托咪定
信号通路
氧化应激
炎症
凋亡
ischemia-reperfusion injury
dexmedetomidine
signaling pathway
oxidative stress
inflammation
apoptosis
