内质网应激与缺血后处理的心肌保护  

Endoplasmic reticulum stress and the cardioprotection of ischemic postconditioning

作　　者：杨海燕[1] 刘新伟[1] 

机构地区：[1]重庆医科大学附属第一医院麻醉科,400016

出　　处：《国际麻醉学与复苏杂志》2010年第3期244-247,共4页International Journal of Anesthesiology and Resuscitation

摘　　要：内质网应激（endoplasmic reticulum stress,ERS）是细胞对各种伤害性刺激的适应性反应.在心肌缺血/再灌注（ischemia/reperfusion,I/R）过程中,过度的ERS引起心肌细胞凋亡导致心肌损伤.缺血后处理（ischemic postconditioning,I-postC）是心肌对抗I/R损伤的内源性保护现象,可通过多条信号转导途径发挥心肌保护作用,对ERS的调节是其重要方面.现将从ERS的角度探讨I-postC的心肌保护机制.Endoplasmic reticulum stress is the cell adaptation reaction for a variety of noxious stimulation. But excessive endoplasmic reticulum stress can induce apoptosis and further lead to myocardium injury in the process of ischemia-reperfusion. lschemic postconditioning is a phenomenon of endogenous protection which attenuates reperfusion injury by several signal transduction pathways, and regulation of endoplasmic reticulum stress is an important aspect. This review will discuss the cardioprotection mechanisms of ischemic postconditioning from endoplasmic reticulum stress.

关 键 词：内质网应激 凋亡 缺血后处理 信号转导 

分 类 号：R285.5[医药卫生—中药学]