活性氧与内质网应激  

ROS and endoplasmic reticulum stress

作　　者：周映彤[1] 肖洪彬[1] 毕明刚[2] 

机构地区：[1]黑龙江中医药大学药理毒理研究中心,黑龙江哈尔滨150000 [2]中国医学科学院药用植物研究所,北京100193

出　　处：《中国药理学通报》2011年第5期597-600,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No30873090)

摘　　要：内质网(endoplasmic reticulum,ER)是细胞加工蛋白质和贮存Ca2+的主要场所,对应激极为敏感,其功能紊乱时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,称为内质网应激(endoplasmic reticulum stress,ERS)。活性氧(reactive oxygen species,ROS)作为第二信使,在细胞生物学功能的调节中起着重要作用。细胞内氧化还原状态的改变促进了ROS的产生和凋亡诱导因子的激活,致使细胞凋亡的同时又加剧了细胞内氧化还原状态的改变。研究发现细胞内氧化还原水平的改变在ERS介导的细胞凋亡过程中承担重要的角色,推测ROS可能是ERS介导的凋亡通路的上游信号分子,该文就ROS与ERS之间的关系作一综述。The endoplasmic reticulum（ER） is a major site for protein processing and Ca^2＋ storage and it is extremely sensitive to the stress.In the state of dysfunction,unfolded or misfolded protein accumulation and Ca^2＋ disbalance occur,known as endoplasmic reticulum stress（ERS）.Reactive oxygen species（ROS）,as a second messenger plays an important role in the regulation of biological function in cells.Intracellular changes in redox state promote the generation of ROS and the activation of apoptosis inducing factor,leading to apoptosis which in turn exacerbate the intracellular redox state change.Recent studies have found that intracellular redox changes in the level of ERS mediated apoptosis assumes an important role in the process,and it is speculated that ROS is the upstream signal molecule in ERS-mediated apoptosis pathway.This paper provides a review of the relationship between ROS and ERS.

关 键 词：活性氧 内质网应激 未折叠蛋白反应 钙 细胞凋亡 氧化还原 

分 类 号：R-05[医药卫生] R329.24