药学服务与研究
藥學服務與研究
약학복무여연구
PHARMACEUTICAL CARE AND RESEARCH
2009年
6期
452-454
,共3页
依达拉奉%脑缺血%内质网应激%葡萄糖调节蛋白-78%caspase-12
依達拉奉%腦缺血%內質網應激%葡萄糖調節蛋白-78%caspase-12
의체랍봉%뇌결혈%내질망응격%포도당조절단백-78%caspase-12
edaravone%cerebral ischemia%endoplasmic reticulastress%glucosregulation protein-78%caspase-12
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、10.0 mg/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.
目的:研究依達拉奉對大鼠腦組織缺血急性期引起的內質網應激(endoplasmic reticulum stress,ERS)的保護作用.方法:採用線栓法製備大鼠右大腦中動脈供血區缺血模型,通過腦組織含水量的測定和神經功能缺損評分來評價不同劑量(3.0、10.0 mg/kg)依達拉奉的腦保護作用,併通過進一步檢測與ERS相關的分子葡萄糖調節蛋白-78(GRP78)和caspase-12的錶達量變化,來觀察依達拉奉的腦保護作用與腦組織ERS的相關性.結果:不同劑量依達拉奉均可以使腦缺血急性期水腫的腦組織含水量減少,使大鼠神經功能評分改善,使大鼠腦缺血後高錶達的GRP78齣現下調,caspase-12的激活也受到抑製.結論:依達拉奉具有一定的腦保護作用,其機製可能與抑製腦組織缺血時的ERS有關.
목적:연구의체랍봉대대서뇌조직결혈급성기인기적내질망응격(endoplasmic reticulum stress,ERS)적보호작용.방법:채용선전법제비대서우대뇌중동맥공혈구결혈모형,통과뇌조직함수량적측정화신경공능결손평분래평개불동제량(3.0、10.0 mg/kg)의체랍봉적뇌보호작용,병통과진일보검측여ERS상관적분자포도당조절단백-78(GRP78)화caspase-12적표체량변화,래관찰의체랍봉적뇌보호작용여뇌조직ERS적상관성.결과:불동제량의체랍봉균가이사뇌결혈급성기수종적뇌조직함수량감소,사대서신경공능평분개선,사대서뇌결혈후고표체적GRP78출현하조,caspase-12적격활야수도억제.결론:의체랍봉구유일정적뇌보호작용,기궤제가능여억제뇌조직결혈시적ERS유관.
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.
