首页 | 本学科首页   官方微博 | 高级检索  
检索        

依达拉奉对大鼠脑缺血急性期内质网应激的保护作用
引用本文:许春立,陶沂.依达拉奉对大鼠脑缺血急性期内质网应激的保护作用[J].药学服务与研究,2009,9(6):452-454.
作者姓名:许春立  陶沂
作者单位:第二军医大学长海医院神经内科,上海,200433
摘    要:目的:研究依达拉奉对大鼠脑组织缺血急性期引起的内质网应激(endoplasmic reticulum stress,ERS)的保护作用。方法:采用线栓法制备大鼠右大脑中动脉供血区缺血模型,通过脑组织含水量的测定和神经功能缺损评分来评价不同剂量(3.0、10.0mg/kg)依达拉奉的脑保护作用,并通过进一步检测与ERS相关的分子葡萄糖调节蛋白-78(GRP78)和caspase-12的表达量变化,来观察依达拉奉的脑保护作用与脑组织ERS的相关性。结果:不同剂量依达拉奉均可以使脑缺血急性期水肿的脑组织含水量减少,使大鼠神经功能评分改善,使大鼠脑缺血后高表达的GRP78出现下调,caspase-12的激活也受到抑制。结论:依达拉奉具有一定的脑保护作用,其机制可能与抑制脑组织缺血时的ERS有关。

关 键 词:依达拉奉  脑缺血  内质网应激  葡萄糖调节蛋白-78  caspase-12

Protective effects of edaravone against ischemia-induced endoplasmic reticulum stress in rats
XU Chun-li,TAO Yi.Protective effects of edaravone against ischemia-induced endoplasmic reticulum stress in rats[J].Pharmaceutical Care and Research,2009,9(6):452-454.
Authors:XU Chun-li  TAO Yi
Institution:(Department of Neurology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China)
Abstract:Objective:To investigate the protective effects of edaravone against endoplasmic reticulum stress induced by brain ischemia.Methods:Focal cerebral ischemia model was made by Longa method in Sprague-Dawley rats.Water content of rat brain tissue was determined and neurological deficits after ischemia were assessed and scored.Western blot was used to determine the expression of GRP78 and activity of caspase-12.Results:The expression of GRP78 was elevated at 2,6,12,24 and 48 h after ischemia,and restored at 72 h;furthermore,caspase-12 was activated at 24 and 48 h after ischemia.Edaravone could significantly down-regulate the high expression of GRP78 and repress the activation of caspase-12.Conclusion:Edaravone has protective effects against brain ischemia and the mechanism of protective effect is possibly related to inhibition of endoplasmic reticulum stress.
Keywords:caspase-12  edaravone  cerebral ischemia  endoplasmic reticulastress  glucosregulation protein-78  caspase-12
本文献已被 维普 万方数据 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号