摘要
缺血性脑卒中是一种常见的脑血管疾病,其发病率逐年上升,是全球范围内导致死亡和残疾的主要原因之一。β_(2)肾上腺素能受体(β_(2)-adrenergic receptor,β_(2)-AR)属于G蛋白耦联受体(G protein-coupled receptor,GPCR)家族。这类受体在细胞膜上发挥作用,通过结合特定的配体如肾上腺素(epinephrine,E)和去甲肾上腺素(norepinephrine,NE)调控细胞内信号转导。近年研究发现,β_(2)-AR信号通路在缺血性脑卒中中表现出多方面的神经保护作用,如促进神经营养因子分泌、减轻炎症反应、抗细胞凋亡、减轻兴奋性毒性以及修复血脑屏障等。还有研究表明β_(2)-AR的激活在卒中后肺炎中发挥作用。β_(2)-AR基因多态性也与缺血性脑卒中风险之间存在显著关联。本文系统综述β_(2)-AR信号通路在缺血性脑卒中中的作用机制,旨在为防治缺血性脑卒中提供理论基础。
Ischemic stroke is a common cerebrovascular disease with an increasing incidence year by year,and it remains one of the leading causes of death and disability worldwide.Theβ_(2)-adrenergic receptor(β_(2)-AR),a member of the G protein-coupled receptor(GPCR)family,functions on the cell membrane by binding to specific ligands such as epinephrine(E)and norepinephrine(NE),thereby regulating intracellular signal transduction.Recent studies have revealed that theβ_(2)-AR signaling pathway exerts multifaceted neuroprotective effects on ischemic stroke,including promoting the secretion of neurotrophic factors,mitigating inflammatory responses,inhibiting apoptosis,reducing excitotoxicity,and repairing the blood-brain barrier.Furthermore,research suggests thatβ_(2)-AR activation plays a role in post-stroke pneumonia.Additionally,β_(2)-AR gene polymorphisms have been significantly associated with the risk of ischemic stroke.This article reviews the mechanisms of theβ_(2)-AR signaling pathway in ischemic stroke,aiming to provide a theoretical foundation for the prevention and treatment of this condition.
作者
张爽
王可
王月
刘倩倩
何治
ZHANG Shuang;WANG Ke;WANG Yue;LIU Qian-Qian;HE Zhi(Third-grade Pharmacological Laboratory on Traditional Chinese Medicine,National Administration of Traditional Chinese Medicine,China Three Gorges University,Yichang 443002,China;Health Medical College,China Three Gorges University,Yichang 443002,China;Jiaxing University College of Medicine,Jiaxing 314000,China)
出处
《生理学报》
北大核心
2026年第2期270-282,共13页
Acta Physiologica Sinica
基金
supported by the Youth Fund Project of the National Natural Science Foundation of China(No.82204837)
Zhejiang Provincial Natural Science Foundation(No.LQ23H290004)
the Key Project of Zhejiang Provincial Natural Science Foundation(No.LZ25H310002)
the General Project of the National Natural Science Foundation of China(No.82073824).#These authors contributed equally to this work.
