摘要
目的探讨脑缺血预处理对脑功能的保护作用及其可能的机制。方法将 71只wistar大鼠随机分为 6组 :A组 (空白对照组 ,n =9)、B组 (实验对照组 ,n =12 )、C组 (致死性缺血组 ,n =9)、D组 (缺血预处理组 ,n =12 )、E组 (CPA组 ,n =16 )、F组 (DPCPX组 ,n =16 ) ,参照 pulsinelli的四血管闭塞法制作大鼠全脑缺血模型。对A、B、C、D四组动物的双侧颈总动脉分别用微型动脉瘤夹予以夹闭或松开 ,以达到实验所需的脑缺血时间或再灌注时间 ;E组、F组动物分别于缺血前不同时间腹腔注射CPA或DPCPX进行药物预处理。各实验组于特定缺血阶段后再灌注 3d或 7d取材 ,采用热休克蛋白的免疫组织化学技术和形态学方法对各组海马CAⅠ区神经元进行了研究。结果D组 (脑缺血预处理组 )和E组 (CPA组 )海马CAⅠ区神经元大部分保持完好 ,神经元密度均高于没有进行预处理的C组 (致死缺血组 ,P <0 .0 1) ,但三组海马CAⅠ区均可观察到热休克蛋白 (HSP) 70的表达 ;F组 (DPCPX组 )海马CAⅠ区神经元大片毁损 ,神经元密度低于A组、D组、E组 (P <0 .0 1) ,免疫组织化学结果为阴性。结论脑缺血预处理或预防性应用腺苷A1受体激动剂对脑功能具有明显的保护效应。
ObjectivesTo explore the protection of brain function by cerebral ischemic preconditioning and the mechanisms involved in ischemic tolerance.MethodsSeventy four adult Wistar rats were randomly divided into six group:①Group A (blank control); Group B (experiment control); Group C (lethal ischemia); Group D (ischemic preconditioning);Group E (N 6 cyclopentyladenosine,CPA preconditioning); Group F(8 cyclopenty 1,3 dipropylxcenthine,DPCPX preconditioning). Brain ischemia model was induced by 4 vessel occlusion method as described by Pulsinelli et al.Both common carotid arteries of rats in Groups A,B,C,D were occluded or released with miniature aneurysm clips in order to control the time of brain ischemia or reperfusion; In Group E and F, two drugs? CPA and DPCPX preconditionings were carried out i.p. respectively in different duration before ischemia. was established .The brain tissues in each group were resected following reperfusion for 3 or 7 days after the special ischemic phases ,and neurons from the CA Ⅰ region of hippocampus were studied by morphological and immunohistochemical techniques of heat shock protein(HSP) respectively.ResultsThe CA Ⅰ region neurons of hippocampus in Group D (ischemic preconditioning) and Group E(CPA preconditioning) were protected fairly well, and results of their neuronal density were significantly higher than those of Group C (lethal ischemia)(P<0.01), but expressions of HSP were visible within CA Ⅰ region of hippocampus in all three groups. The CA Ⅰ region neurons of hippocampus in Group F (DPCPX preconditioning) were destroyed severely, with negative immunoreaction for HSP 70; and their neuronal density was the lowest as compared with that in Groups A,D and E (P<0.01).ConclusionCerebral ischemic preconditioning or prophylactic application with adenosine receptor A 1 agonist can produce obvious protective effects on brain function.
出处
《医学临床研究》
CAS
2003年第8期574-577,共4页
Journal of Clinical Research
