摘要
目的 研究开放线粒体 ATP敏感性钾通道对大鼠局灶性脑缺血再灌注损伤的作用。方法 采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型 ,将 38只大鼠随机分成 4组 :假手术组 (S)、缺血组 (I)、缺血 +二氮嗪组 (D)、缺血 +二氮嗪 +5 - HD组 (DH)。观察各组脑梗死体积和线粒体标志酶活性变化。结果 与 I组比较 ,D组脑梗死体积明显减少 (自 2 3.5 7± 7.83%减至 8.16± 3.81% ) ,线粒体标志酶活性明显增高 ,差异具有显著性 (P<0 .0 5 ) ,DH组与 I组比较无明显差异 (P>0 .0 5 )。结论 二氮嗪对大鼠局灶性脑缺血再灌注损伤具有保护作用 ,其机制与开放线粒体 ATP敏感性钾通道 。
Objective To investigate effects of opening mitochondrial ATP-sensitive K + (mitoK ATP) channels against brain damage after middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats.Methods The rat focal cerebral ischemia and reperfusion model was performed by 2h thread embolism of middle cerebral artery and 22h of reperfusion(I/R).Diazoxide,a selective opener of mitoK ATP or 5-hydroxydecanoate(5-HD,a selective blocker of mitoK ATP or saline was infused into the right lateral ventricle 30min before MCAO.38 rats were assigned to 4 groups randomly,which received 1 of the following pretreatments before I/R:sham operation;saline;diazoxide;coapplication of 5-HD.Infarct size (IS) was measured by tetrazolium staining,activity of succinate dehydrogenase(SDH)and cytochrome oxidase(CO)was detected by enzyme histochemistry.Results Diazoxide caused a decrease in IS(P<0.05),increased the activity of SDH and CO(P<0.05).The effect of diazoxide was completely abolished by 5-HD(P<0.05). Conclusion Diazoxide play a benefit role in rat focal cerebral ischemia and reperfusion injury through opening mitoK ATP,preserving the function of the mitochondria.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2004年第2期104-106,共3页
Journal of Apoplexy and Nervous Diseases
基金
海南省教育厅资助项目 (Hjkj2 0 0 3 2 3 )
