【摘要】 目的探讨易卒中型肾血管性高血压大鼠(SPRHR)大脑皮质梗死后丘脑腹后核继发性损害及其机制,以为脑梗死临床康复治疗提供理论依据。方法采用易卒中型肾血管性高血压大鼠制备大脑中动脉闭塞(MCAO)模型,应用尼氏染色TUNEL法和免疫组织化学染色检测大鼠梗死侧丘脑腹后核神经元形态、凋亡细胞数目,以及微管相关蛋白-2、胶质纤维酸性蛋白和少突胶质细胞特异性标志蛋白RIP的表达水平。结果与假手术组比较,手术后1周,MCAO组大鼠梗死侧丘脑腹后核正常神经元数目减少38.31%(P<0.01);至手术后4周减少73.49%(P<0.01)。与假手术组比较,手术后1周,MCAO组大鼠梗死侧丘脑腹后核即可见凋亡细胞(P<0.01),至手术后2周和4周,凋亡细胞持续存在,并可见坏死细胞。与假手术组比较,手术后1周,MCAO组大鼠梗死侧丘脑腹后核微管相关蛋白-2表达水平无明显变化(P>0.05),而胶质纤维酸性蛋白和少突胶质细胞特异性标志蛋白RIP表达水平明显升高(均P<0.01);至手术后2周和4周,微管相关蛋白-2表达水平逐渐降低(P=0.000,0.000),而胶质纤维酸性蛋白(P=0.000,0.000)和少突胶质细胞特异性标志蛋白RIP(P=0.012,0.047)表达水平则逐渐升高且呈持续高表达。结论大脑皮质梗死后同侧丘脑腹后核神经元呈进行性死亡。梗死侧丘脑神经元凋亡、延迟性星形胶质细胞反应性增生、少突胶质细胞增生及其磷脂蛋白持续高表达可能是造成梗死侧丘脑腹后核继发性损害的重要原因。更多还原

【Abstract】 Objective To investigate the secondary injury of ipsilateral ventral posterior nuclei of tha-lamus(VPN) and its mechanism after cerebral cortical infarction in stroke-prone renovascular hypertensive rats(SPRHR) and to provide the evidence of clinical rehabilitation in cerebral cortical infarction.Methods Middle cerebral artery occlusion(MCAO) models were established with SPRHR.Nissl staining,TUNEL method and immunohistochemistry staining were used to obeserve the neuronal phenotype,detect the number of cell apoptosis and determine the expression of microtubule-associated protein-2(MAP-2),glial fibrillary acidic protein(GFAP) and RIP(a mark of oligodendrocytes) in the ipsilateral VPN after cerebral cortical in-farction.Results Compared with sham-operation group,the number of normal neurons in the infarcted isp-silateral VPN decreased by 38.31% and 73.49% at 1 and 4 week after operation in MCAO group(P < 0.01,re-spectively).In comparison with sham-operation group,cell apoptosis in the infarcted ipsilateral VPN could be detected at 1 week after operation and sustained at 2 and 4 week after operation in MCAO group.Cell necrosis was also found at 2 and 4 week after operation in MCAO group.There was no significant difference of the expression of MAP-2 between MCAO group and sham-operation group at 1 week after operation(P > 0.05),while the expressions of GFAP and RIP significantly increased at 1 week after operation in MCAO group(P < 0.01,for all).Until 2 and 4 week after operation the expression of MAP-2 gradually decreased(P = 0.000,0.000),and the expression of GFAP(P = 0.000,0.000) and RIP(P = 0.012,0.047)gradually increased and kept at high level.Conclusion A progressive neuronal loss was observed in ipsilat-eral VPN after cerebral cortical infarction.Neuron apoptosis,delayed reactive astrocyte hyperplasia,oligoden-drocyte hyperplasia and the persistent high expression of phospholipid protein are confirmed to be important factors for the secondary injury of infarcted ipsilateral VPN.更多还原