摘要
目的:探讨阿司匹林(ASA)对大鼠脑缺血后解偶联蛋白-4(UCP-4)和ATPase-6表达的影响。方法:采用线栓法在血管内堵塞右侧大脑中动脉起始部2 h,制作大脑中动脉支配区缺血模型。随机分为对照组和ASA组(腹腔注射ASA80 mg·kg-1.d-1),每组按再灌注时间0、6、24、48和72 h分为5个亚组。采用间接免疫荧光方法检测UCP-4和ATPase-6表达。结果:UCP-4在缺血后6 h表达增加(P<0.05),随后表达下降,72 h达最低(P<0.01);ATPase-6在缺血6 h后呈下降趋势。与对照组比较,ASA干预后,缺血边缘区UCP-4表达增加,缺血后48 h最为显著(P<0.01);ATPase-6表达下降幅度减少,缺血24 h时最为明显(P<0.01)。结论:ASA增加缺血脑组织线粒体内UCP-4和ATPase-6的表达是其神经保护作用机制之一。
Aim： To investigate the effect of aspirin（ASA） on the expression of uncoupling protein-4（UCP4） and ATPase-6 after reversible focal cerebral ischemia.Methods： To induce temporary ischemia of the right middle cerebral artery territory in rats the filament method was applied endovascularly to occlude the origin of the middle cerebral artery for 2 hours.The rats were randomly divided into two groups： a control group and ASA groups in which the rats were treated once daily with intraperitoneally injection of 80 mg·kg-1 aspirin.Each ASA group was further divided into five subgroups according to reperfusion time of 0 h,6 h,24 h,48 h and 72 h after vessel occlusion.The expression of UCP-4 and ATPase-6 was detected by indirect immunofluorescence.Results： The expression of UCP-4 increased at 6 h after ischemia（P0.05）,decreased thereafter,and reached to the lowest level 72 h after ischemia（P0.01）.The expression of ATPase-6 had a downtrend tendency at 6 h after ischemia.Compared with the control group,ASA treatment markedly induced the expression of UCP-4 and ATPase-6 in the ischemic border zones at 48 h or 24 h after ischemia（P0.01）.Conclusion： Aspirin could enhance the expression of UCP-4 and ATPase-6 after cerebral ischemia,which is one of its neuroprotective mechanisms.
出处
《中国临床神经科学》
2012年第3期258-262,共5页
Chinese Journal of Clinical Neurosciences
基金
辽宁省科技攻关项目资助(编号:2004225003-16)
