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目的:为了解癫痫(Epilepsg,EP)发生后大脑海马区的损害情况,本文采用戊四氮诱导建立大鼠癫痫模型, 采用酶标免疫吸附法(EIA)和免疫组化染色法检测NSE的改变,使用电子显微镜研究超微结构的改变,探讨EP后脑组织的损坏情况。方法:雄性SD大鼠54只,随机分为对照组(A=13)及实验组(41只)。实验组腹腔注射(IP)PTZ 50mg/ kg体重1次,对照组IP生理盐水。根据EP发作分级,0-1级7只,视为B组,立即取脑:2级以上发作34只,随机抽样于EP发作后0h(C=10);6h(D=14);24h(E=10)断头。取脑前抽取躯干血,分离海马。A、D组随机抽取3只进行电镜观察。采用EIA法测试血清和海马NSE-值;以S-P免疫组化染色法染色,观察各组大鼠海马的NSE表达。结果:实验组海马和血清的NSE均明显高于对照组:即使无EP大发作,但有兴奋症状的大鼠,NSE亦高于对照组,表明也有脑组织损害。免疫组化染色显示:对照组海马组织几乎未见NSE的表达,即大发作后海马的NSE表达明显增加,但随时间推移而降低。电镜观察发现EP后大鼠海马CA1区的神经元细胞出现水肿、基质密度变淡、微丝溶解消失、细胞器减少、毛细血管周围间隙扩大等明显改变。结论:EP发作对大鼠海马区神经细胞造成了明显的损害。
OBJECTIVE: To understand the damage of hippocampus in epileptic brain after Epilepsy (EP), a rat model of epilepsy induced by pentylenetetrazol was established in this study. The changes of NSE were detected by enzyme-linked immunosorbent assay (EIA) and immunohistochemistry , The use of electron microscopy ultrastructural changes to explore the damage of brain tissue after EP. Methods: 54 male SD rats were randomly divided into control group (A = 13) and experimental group (41). Experimental group intraperitoneal injection (IP) PTZ 50mg / kg body weight once in the control group IP saline. According to the classification of EP seizures, 0-1 grade 7, regarded as group B, immediately take the brain: 34 cases above grade 2, random sampling in EP 0h (C = 10); 6h E = 10) decapitation. Taken from the brain trunk blood, separation of the hippocampus. Groups A and D were randomly selected for electron microscopy. NSE-values of serum and hippocampus were measured by EIA method. NSE expression in hippocampus of each group was observed by S-P immunohistochemical staining. Results: The NSE in the hippocampus and serum of the experimental group were significantly higher than that of the control group. NSE was higher in the rats with excitatory symptoms than those in the control group, indicating that there was also brain damage. Immunohistochemical staining showed that there was almost no NSE expression in the hippocampus of the control group, that is, the NSE expression in the hippocampus significantly increased after the major episode but decreased with time. Electron microscopy showed that edema of neurons in hippocampal CA1 region was observed in EP rats. The matrix density became fainter, the fibrinolytic disappeared, the number of organelles decreased and the space around the capillaries enlarged obviously. Conclusion: The onset of EP caused obvious damage to the neurons in the hippocampus of rats.