二价金属离子转运体-1介导的神经元铁蓄积在脑缺血后认知功能障碍发生机制中研究  

The research for mechanisms of cognitive dysfunction induced by divalent metal transporter-1-mediated neurons iron accumulation after cerebral ischemia

作　　者：王红柏[1] 王海云[1] 

机构地区：[1]天津医科大学总医院麻醉科,300052

出　　处：《国际麻醉学与复苏杂志》2014年第11期1037-1040,共4页International Journal of Anesthesiology and Resuscitation

摘　　要：背景 铁作为一种必需营养元素,参与人体的多种生理过程,缺铁会导致多种疾病的发生.但是,近来大量研究证明铁在细胞内过量蓄积,会产生细胞毒性反应,损害细胞功能.二价金属离子转运体-1 （divalent metal transporter-1,DMT1）是一种以转运亚铁离子为主的膜金属离子转运蛋白,其在肠道非蛋白铁的吸收和细胞铁的摄取等生理过程中起着重要的作用,是机体铁平衡代谢的一个极其重要的调节因子.近来研究发现,当发生脑梗死时,哺乳动物神经元出现铁蓄积,而通过有效措施抑制DMT1的功能,则神经元对铁的摄取减少,改善认知功能.因此,学者认为,哺乳动物大脑发生缺血性损伤后,DMT1表达增多,导致细胞内铁进一步增加,加重神经元损伤,从而形成恶性循环,降低哺乳动物的认知功能.目的 探讨DMT1介导的铁蓄积在脑缺血后认知功能障碍发生中的作用.内容 综述铁的吸收和释放机制、DMT1的结构和功能以及铁蓄积对脑缺血后认知功能的影响及机制.趋向 探讨DMT1在脑缺血性损害病理生理学机制中的作用,为临床上减轻脑梗死导致的认知功能障碍,提供了新的思路和方法.Background Recent studies demonstrate that iron accumulation in cells can produce toxicity and impair the function of cells.Divalent metal transporter-1 （DMT1）,a membrane protein transporting metal ions,plays a pivotal role in intestinal nonheme-iron absorption and iron acquisition by cells.Recent data shows that when cerebral artery infarction occurs,thc iron accumulates in neurons,whereas inhibition of DMT1 by some effective approaches decreases the iron accumulation in neurons and improves mammal＇s cognitive state.Objective To assess the mechanisms of cognitive dysfunction induced by DMT1-mediated iron accumulation after cerebral ischemia.Content This review presents the mechanisms of iron absorption and releasing for neurons,molecular structures and physiological functions of DMT1,effects of DMT1 on iron accumulation after cerebral ischemia,effects and mechanisms of iron accumulation on cognition after cerebral ischemia.Trend By assessing the role of pathophysiological mechanisms of DMT1 after cerebral ischemia,it is possible to provide novel approach relieving cognitive dysfunction after cerebral artery infarction.

关 键 词：二价金属转运体 脑缺血性损伤 铁蓄积 认知障碍 

分 类 号：R614[医药卫生—麻醉学]