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目的 探讨海马胶质细胞增生和谷氨酸转运异常在铁离子诱发创伤性癫大鼠发病机制中的作用,以及胶质细胞增生对谷氨酸转运体表达的影响。方法 36只SD大鼠随机分3组,A组单侧杏仁核内注射生理盐水,B组仅注射氯化铁,C组注射氯化铁后,静脉注射含7β羟基胆固醇的脂质包被微泡。动态观察大鼠脑电图和行为改变,并用免疫组化、免疫印迹方法观察鼠脑海马胶质纤维酸性蛋白(glialfibrillaryacidicprotein,GFAP)在注射氯化铁后15d的表达,同时应用逆转录聚合酶链反应(RT -PCR)检测双侧海马谷氨酸天门冬氨酸转运体(GLAST)、谷氨酸转运体1 (GLT1 )和兴奋性氨基酸载体1(EAAC1)mRNA的表达。结果 A组大鼠行为学和脑电图表现无明显改变;B组大鼠致成功92%,致潜伏期为( 6 .09±0 .37 )d;C组致比例降低到67%,致潜伏期延长至(10. 07±0. 56)d。致大鼠抽搐发作的同时记录到阵发的节律性的高幅棘波和尖波。B组大鼠双侧海马GFAP表达均比A组明显增高(P<0 05),C组双侧海马GFAP表达比B组低50% ~60%。与A组比较,B组大鼠双侧海马GLASTmRNA表达显著降低(P<0 .05),而EAAC1mRNA表达增高(P<0 .05);C组双侧海马GLASTmRNA表达与A组无明显差异,而GLT1和EAAC1均比A组明显增高(P<0. 05)。结论 胶质细胞的增生和GLAST的下调可能参与
Objective To investigate the role of abnormal hippocampal astrocytes and glutamate transport in pathogenesis of iron-induced traumatic epilepsy in rats and the effect of glial cell proliferation on glutamate transporter expression. Methods Thirty-six SD rats were randomly divided into three groups: group A received unilateral amygdala saline injection, group B received only ferric chloride, group C received ferric chloride, and then received intravenous injection of 7β-hydroxycholesterol- bubble. The electroencephalogram and behavioral changes were observed dynamically. The expression of glial fibrillary acidic protein (glial fibrillary acidic protein GFAP) in hippocampus was observed 15 days after injection of ferric chloride by immunohistochemistry and immunoblotting. The expression of glial fibrillary acidic protein (GLAST), glutamate transporter 1 (GLT1) and excitatory amino acid carrier 1 (EAAC1) mRNA in bilateral hippocampus were detected by RT-PCR. Results The behavior and electroencephalogram (EEG) performance of group A were not changed obviously. The success rate of group B was 92%, the latency was (6 .09 ± 0.37) d and the proportion of group C was 67% , Caused by the incubation period was prolonged to (10. 07 ± 0. 56) d. Induced 抽 rat seizures at the same time recorded the rhythms of intermittent high spikes and spikes. GFAP expression in bilateral hippocampus in group B was significantly higher than that in group A (P <0.05). GFAP expression in bilateral hippocampus in group B was 50% -60% lower than that in group B. Compared with group A, the expression of GLAST mRNA in bilateral hippocampus of group B was significantly lower than that in group A (P <0.05), while the expression of EAAC1 mRNA in group B was significantly higher than that of group A (P <0.05) The GLT1 and EAAC1 were significantly higher than the A group (P <0. 05). Conclusion Glial cell proliferation and down-regulation of GLAST may be involved