【作者】 王粤；

【导师】 郭云良；

【作者基本信息】 青岛大学 ， 神经病学， 2003， 硕士

【摘要】 目的：观察大鼠脑缺血再灌流损伤脑组织神经元特异性烯醇化酶(NSE)、S-100β蛋白的变化规律及其意义；探讨肌苷对缺血性脑损伤的作用机制。 方法：成年健康雌性SD大鼠68只应用线栓法建立大脑中动脉缺血(MCAO)再灌流模型，随机分为对照组(腹腔注射生理盐水)和治疗组(腹腔注射肌苷)，每组再随机分为脑缺血1.5h再灌流2h、6h、12h、1d、2d、3d、7d、14d组，每组4只，另取4只作假手术组。应用神经功能等级评分观察脑缺血再灌流后行为功能的恢复；免疫组化法检测脑缺血再灌流各时间点脑组织中NSE和S-100β的动态变化。 结果：①对照组与治疗组在治疗前神经功能等级评分相同，治疗后均于再灌流3d、7d、14d功能恢复、等级评分减低，与治疗前比有显著意义；治疗组在7d、14d等级评分较对照组显著性降低(P＜0.05)。②NSE：假手术组在皮层和纹状体区，NSE呈基础水平表达，两侧对称；对照组缺血侧NSE的免疫阳性反应于脑缺血再灌流后12h明显增强并达高峰(P＜0.05)，随时间(1d～7d)推移而逐渐下降，至14d降至假手术组水平；治疗组NSE的免疫阳性反应变化趋势同对照组，组间各时间点增加了脑组织中NSE蛋白表达水平，较对照组显著升高(P＜0.05)。两组中皮层区NSE的免疫阳性反应均高于纹状体区。③S-100β：假手术组在皮层和纹状体区，S-100β呈基础水平表达，两侧对称；对照组缺血侧S-100β的免疫阳性反应于脑缺血再灌流后12h明显增强(P＜0.05)，随时间(1d～3d)推移而逐渐增强，3d达高峰，7d时有所下降，与假手术组相比差异仍有显著意义(P＜0.05)，14d降至假手术组水平；在治疗组，S-100β的免疫阳性反应趋势同对照组，但治疗组脑组织中S-100β蛋白表达水平较对照组显著升高(P＜0.05)。与NSE相比，S-100β的表达高峰时间落后。中文摘要 结论脑缺血再灌流损伤后大鼠神经功能有自动恢复的趋势，脑组织NSE、S一100p蛋白表达增强;肌昔对缺血性脑损伤的功能恢复有一定的促进作用，其机制可能与增加脑组织中NSE和S一loop蛋白的表达有关。更多还原

【Abstract】 Objective: To observe the expression and significance of neuron-specific enolase (NSE) and S-100 β in the cerebral tissue after reperfusion of focal cerebral ischemia in rats; To explore the effect of Inosine on hypoxic-ischemic brain damage.Methods: The reperfusion of focal cerebral ischemia models were established with SD rats, which were divided into controlled group (saline solution was injected intraperitoneally) and treatment group (Inosine was injected intraperitoneally). Each group was divided into eight subgroups which consisted of 4 rats. Neurological grade evaluation was used to examine the behavioral recovery on these rats. At 2h, 6h, 12h, ld, 2d, 3d, 7d, 14d after reperfusion of MCA, immunohistochemical technique was used to investigate the dynamic changes of NSE and S-100 β in cerebral tissue.Results: (1)There was improvement in the score of neurologic grade in Inosine treatment group at 7d and 14d after reperfusion when compared with controlled group. (2) NSE: The expression of NSE in cerebral cortex and striatum was low in sham-operate group. In controlled group, the peak expression of NSE occurred at 12h after reperfusion and its expression decreased gradually (ld-7d). At 14d it decreased to controlled level, in treatment group, the change of NSE was similar to the controlled group. The use of Inosine could increase the expression of NSE. In the two groups, the expression of NSE in cerebral cortex was higher than that in striatum. (3)S-100 β : The expression of S-100 β in cerebral cortex and striatum was low in sham-operate group. In controlled group, the expression of S-100 P increased at 12h and continued to increase from 1d to 3d. Thepeak expression occurred at 3d, it decreased at 7d, and to controlled group level at 14d. In treatment group, the change of S-100 β was similar to that of the control group. The use of Inosine could increase the expression of S-100 β .Compared with NSE, the time of peak expression of S-100 β was later. Conclusion: The expression of NSE and S-100β increased significantly in the cerebral tissue after reperfusion of focal cerebral ischemia; It is suggested that Inosine could protect against hypoxic-ischemic brain damage, whose role might be reflected by increasing the expression of NSE and S-100 β.Postgraduate: Wang Yue (Specialty of Neurology)Directed by Guo Yunliang更多还原