国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
International Journal of Anesthesiology and Resuscitation
2015年
9期
839-842
,共4页
HOE-642%Na+/H+交换蛋白%线粒体通透性转换孔%缺血性脑损伤
HOE-642%Na+/H+交換蛋白%線粒體通透性轉換孔%缺血性腦損傷
HOE-642%Na+/H+교환단백%선립체통투성전환공%결혈성뇌손상
HOE-642%Na+/H+ exchanger%Mitochondrial permeability transition pore%Cerebral ischemic injury
背景 Na+/H+交换蛋白(Na+/H+ exchanger,NHE)是一种膜蛋白,维持着细胞内正常的pH值和容量.缺血后NHE的活化可通过Na+、Ca2+介导的毒性效应引起缺血性脑损伤.NHE-1是神经系统中最丰富的NHE亚型.高选择性NHE-1抑制剂HOE-642能降低细胞质内Na+、Ca2+超载、线粒体Ca2+超载和细胞死亡,抑制小胶质细胞的激活和促炎症反应.此外,HOE-642还可以改善神经功能. 目的 对HOE-642在缺血性脑损伤中的神经保护作用机制进行综述. 内容 整理和阐述NHE的结构、功能和组织分布以及HOE-642对缺血性脑损伤的神经保护作用机制. 趋向 随着对于缺血性脑损伤的的深入研究,HOE-642的神经保护作用机制将不断被完善,特别是其对于线粒体通透性转换孔(mitochondrial permeability transition pore,mPTP)的影响.
揹景 Na+/H+交換蛋白(Na+/H+ exchanger,NHE)是一種膜蛋白,維持著細胞內正常的pH值和容量.缺血後NHE的活化可通過Na+、Ca2+介導的毒性效應引起缺血性腦損傷.NHE-1是神經繫統中最豐富的NHE亞型.高選擇性NHE-1抑製劑HOE-642能降低細胞質內Na+、Ca2+超載、線粒體Ca2+超載和細胞死亡,抑製小膠質細胞的激活和促炎癥反應.此外,HOE-642還可以改善神經功能. 目的 對HOE-642在缺血性腦損傷中的神經保護作用機製進行綜述. 內容 整理和闡述NHE的結構、功能和組織分佈以及HOE-642對缺血性腦損傷的神經保護作用機製. 趨嚮 隨著對于缺血性腦損傷的的深入研究,HOE-642的神經保護作用機製將不斷被完善,特彆是其對于線粒體通透性轉換孔(mitochondrial permeability transition pore,mPTP)的影響.
배경 Na+/H+교환단백(Na+/H+ exchanger,NHE)시일충막단백,유지착세포내정상적pH치화용량.결혈후NHE적활화가통과Na+、Ca2+개도적독성효응인기결혈성뇌손상.NHE-1시신경계통중최봉부적NHE아형.고선택성NHE-1억제제HOE-642능강저세포질내Na+、Ca2+초재、선립체Ca2+초재화세포사망,억제소효질세포적격활화촉염증반응.차외,HOE-642환가이개선신경공능. 목적 대HOE-642재결혈성뇌손상중적신경보호작용궤제진행종술. 내용 정리화천술NHE적결구、공능화조직분포이급HOE-642대결혈성뇌손상적신경보호작용궤제. 추향 수착대우결혈성뇌손상적적심입연구,HOE-642적신경보호작용궤제장불단피완선,특별시기대우선립체통투성전환공(mitochondrial permeability transition pore,mPTP)적영향.
Background Na+/H+ exchanger (NHE) is a membrane protein,and responsible for maintaining normal intracellular pH and cell volume.Activation of NHE after ischemia subsequently causes cerebral ischemic damage via Na+-and Ca2+-mediated toxic effects.NHE-1 is the most abundant isoform in central nervous system.Highly selective NHE-1 inhibitor HOE-642 can decrease the intracellular Na +,Ca2 + overload,mitochondria Ca2 + overload,cell death,suppress microglial activation and proinflammatory responses.In addition,improved functional outcome also follows administration of HOE-642.Objective To review the neuroprotective mechanisms of HOE-642 on cerebral ischemic injury.Content This article reviews the structure,function,tissue distribution of NHE,and the neuroprotective mechanisms of HOE-642 on cerebral ischemic injury.Trend With the indepth study of cerebral ischemic injury,the neuroprotective mechanisms of HOE-642 will continue to be updated,especially for the effects of the mitochondrial permeability transition pore (mPTP).
