内质网是蛋白质合成、加工和转运的主要场所。内质网应激是指缺血缺氧、葡萄糖或营养物质缺乏、药物、毒素等因素破坏内质网的稳态,出现错误折叠与未折叠蛋白在腔内聚集以及Ca2+平衡紊乱的状态。内质网早期或未折叠蛋白反应(unfolded protein response,UPR)能提高细胞在有害因素下的生存能力。但剧烈或者持久的ERS,能诱发凋亡机制。研究表明,脑缺血/再灌注后发生ERS,导致神经细胞凋亡和坏死,是引起再灌注损伤的重要原因。本文对近年来ERS在细胞凋亡调控中的重要作用及脑缺血/再灌注损伤与ERS的关系进行综述,这对脑卒中的理论及临床研究具有重要意义,也给治疗脑卒中的药物发现提供新思路。
Endoplasmic reticulum is the main site of protein synthesis, modification and transport. Endoplasmic reticulum stress (ERS) is defined as a situation of gathering misfolded and (or) unfolded protein in endoplasmic reticulum and the failure of Ca2+ homeostasis. Early ERS will induce unfolded protein response (UPR) which may be protective to cells. On the contrary, longtime strong ERS will induce cell apoptosis, even death. A growing number of studies have suggested that ERS induced neuronal apoptosis was involved in the injury of cerebral ischemia and reperfusion. This review mainly summarizes recently reported discoveries concerning ERS associated with cerebral ischemia and reperfusion, which may reveal novel insight into the basic and clinical research of stroke and provide new ideas for the drug discovery.