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沙鼠脑缺血性再灌注及西比灵干预对PAI-1表达变化的影响
The effects of transient cerebral ischemic reperfusion and flunarizine on the expression of plasminogen activator inhibitor-1 protein in brain tissue of gerbils
【摘要】 目的研究沙鼠脑缺血再灌注后脑内1型纤溶酶原激活物抑制剂(PAI-1)蛋白表达变化,以及西比灵干预的影响。方法制作沙鼠脑缺血再灌注模型,实验前给沙鼠喂食西比灵,分别在缺血再灌注(IR)1、3、7 d,用免疫组织化学方法检测脑内PAI-1蛋白的表达,并与其他各组比较。结果正常对照组与假手术组沙鼠脑组织中有微弱PAI-1的阳性表达。缺血再灌注1、3、7d PAI-1呈阳性或强阳性表达,蛋白的表达随再灌注后时间的延长而递增,7 d达高峰,不同时间点PAI-1的表达差异有统计学意义(P<0.01)。西比灵干预后PAI-1的表达趋势亦同缺血再灌注组,但阳性率高于缺血再灌组,差异有统计学意义(P<0.01)。结论沙鼠脑缺血再灌注可诱导脑组织神经元和胶质细胞表达PAI-1蛋白,西比灵可上调PAI-1蛋白表达而有利于抵御脑缺血再灌注造成的脑损伤。
【Abstract】 Objective To study the effects of transient cerebral ischemic reperfusion(IR) and flunarizine on the expression of plasminogen activator inhibitor-1(PAI-1) protein in brain tissue of gerbils.Methods A cerebral transient ischemic-reperfusion model in gerbils was established by clamping both common carotid.The gerbils were fed with flunarizine before experiment in flunarizine treatment group.The expression of PAI-1 protein in brain tissue was detected by immunohistochemistry technique at the 1,3 and 7 days after IR.Results There was slight expression of PAI-1 protein in the brain tissue of gerbils in the normal control group and sham operation group.Compared with normal control group,the expression of PAI-1 protein in neurons and gliacytes of ischemic gerbils was evidently increased at the 1,3 and 7 days in the cerebral ischemia group(all P<0.01).Compared with cerebral ischemia group,the expression of PAI-1 protein in neurons and gliacytes of gerbils in flunarizine treatment group was significantly increased at the 1,3 and 7 days(all P<0.01).Conclusions The expression of PAI-1 protein in neurons and gliacytes of gerbils is evidently increased following cerebral ischemic reperfusion,and up-regulated with the treatment of flunarizine,which resists the brain injured caused by transient cerebral ischemic reperfusion.
【Key words】 Reperfusion; Brain ischemia; Flunarizine; Plasminogen activator inhibitor 1;
- 【文献出处】 中国医师杂志 ,Journal of Chinese Physician , 编辑部邮箱 ,2006年02期
- 【分类号】R965
- 【下载频次】63