论文部分内容阅读
目的观察新型的谷氨酸转运体抑制剂 TBOA 对全脑缺血性癫癎的发生及神经病理的作用,探索全脑缺血性癫癎的治疗新方法。方法应用稳定可靠的大鼠胸部压迫8min 全脑缺血性癫癎模型,分为缺血癫癎组和 TBOA 治疗组。胸部挤压前3d大鼠侧脑室内注射 TBOA,研究两组癫癎的发生率、海马及皮质病理改变、神经元计数。结果缺血后24h 癫癎发生率在缺血癫癎组为61%,TBOA 治疗组为40%,光镜病理显示,TBOA 治疗组损害程度轻于缺血癫癎组。海马 CAI 区神经元计数:缺血早期(24h,72h 组),缺血癫癎组与 TBOA 治疗组比较无显著性差异,P>0.05;缺血后期(5d,7d 组),缺血癫癎组神经元计数少于TBOA 治疗组,P 均<0.05。皮质区变化规律同海马 CAI 区。结论全脑缺血前应用谷氨酸转运体抑制剂 TBOA 能降低癫癎的发生率,并改善缺血后神经病理损害。
Objective To observe the effect of TBOA, a novel inhibitor of glutamate transporter, on the occurrence and neuropathology of global cerebral ischemic epilepsy and to explore a new method for the treatment of global cerebral ischemic epilepsy. Methods A stable and reliable model of global cerebral ischemic epilepsy was established in 8 min after chest compression in rats. The models were divided into ischemic epilepsy group and TBOA treatment group. Rats were intracerebroventricularly injected with TBOA three days before chest compression to study the incidence of epilepsy, pathological changes in the hippocampus and cortex, and neuron counts. Results The incidence of epilepsy was 61% in ischemic epilepsy group and 40% in TBOA group after ischemia. Pathological examination showed that the damage degree of TBOA group was less than that of ischemic epilepsy group. There was no significant difference between the ischemic epilepsy group and the TBOA treatment group (P> 0.05); the level of neuron in the hippocampal CAI area was significantly higher than that of the TBOA group (P <0.05); in the early stage of ischemia (24h, 72h) Group neurons count less than the TBOA treatment group, P <0.05. Cortical area changes with the hippocampal CAI area. Conclusion The application of glutamate transporter inhibitor TBOA before global cerebral ischemia can reduce the incidence of epilepsy and improve the neuropathological damage after ischemia.