胆碱能抗炎通路在卒中相关性肺炎中的研究进展  

Research progress on cholinergic anti-inflammatory pathway in stroke associated pneumonia

作　　者：凌泽法 王凯 王亚茹 马玉秀 林雨洁 李小梅[1] 刘红[1] Ling Zefa;Wang Kai;Wang Yaru;Ma Yuxiu;Lin Yujie;Li Xiaomei;Liu Hong(Department of Neurology,Heping Hospital Affiliated to Changzhi Medical College,Changzhi,Shanxi 046000,China)

机构地区：[1]长治医学院附属和平医院神经内科,山西长治046000

出　　处：《齐齐哈尔医学院学报》2024年第4期380-385,共6页Journal of Qiqihar Medical University

基　　金：长治医学院青年启动基金(HPYJ201922)。

摘　　要：卒中相关性肺炎(storke-associated pneumonia,SAP)的发病机制并不完全清楚。多项研究提示,卒中诱导的免疫抑制可能参与了SAP的发生,其中下丘脑—垂体—肾上腺轴、交感神经系统和具有胆碱能信号的副交感神经系统在脑卒中后免疫抑制的发生过程中发挥核心作用。卒中后的副交感神经激活能抑制过度炎症反应,保护脑组织,同时也会降低机体对病原菌的抵抗力,增加感染的发生概率。目前胆碱能抗炎通路已经成为SAP的研究热点。本文对胆碱能抗炎通路在卒中相关性肺炎中的机制及干预策略进行综述。The pathogenesis of stroke-associated pneumonia(SAP) is not fully understood.Several studies have suggested that stroke-induced immunosuppression may be involved in the occurrence of SAP.The hypothalamic-pituitary-adrenal(HPA) axis,the sympathetic nervous system(SNS) and the parasympathetic nervous system(PNS) with cholinergic signaling play a central role in the development of post-stroke immunosuppression.Parasympathetic activation after stroke suppresses excessive inflammatory responses and protects brain tissue,and also reduces the body's resistance to pathogenic bacteria and increases the probability of infection.The cholinergic anti-inflammatory pathway has now become a hot topic of research in SAP.This article reviews the mechanisms and intervention strategies of cholinergic anti-inflammatory pathways in stroke-associated pneumonia.

关 键 词：卒中相关性肺炎 免疫抑制 胆碱能抗炎通路 靶向治疗 

分 类 号：R743.3[医药卫生—神经病学与精神病学]