雷公藤内酯醇对匹罗卡品致痫大鼠海马神经元的保护性研究

目的研究雷公藤内酯醇对颞叶癫痫大鼠海马神经元的保护作用及其机制。方法随机将70只生后21 d的雄性Wistar大鼠分为空白对照组10只,癫痫组及雷公藤内酯醇干预组各30只。采用Nissl、FJB染色法观察海马神经元的损伤变化;采用免疫组化法检测海马组织中星形胶质细胞标志物胶质纤维酸性蛋白(GFAP)和小胶质细胞标志物钙离子结合适配器分子1(IBa-1)的表达状况。结果与空白对照组相比,癫痫组和药物干预组海马神经元损伤明显,GFAP、IBa-1呈高表达;与癫痫组相比,药物干预组海马神经元的损伤较小,GFAP及IBa-1表达较低。结论雷公藤内酯醇对癫痫持续状态后海马神经元的损伤有保护性作用,其作用机制可能与雷公藤内酯醇抑制胶质细胞活化抵抗脑内炎症反应有关。

Effect of triptolide on protection of neurons in the hippocampus of epileptic rats induced by lithium chloride-pilocarpine

Objective To investigate the protective effect of triptolide on hippocampal neuronal loss of rats with lithium chloride-pilocarpine-induced temporal lobe epilepticus(TLE) and the possible mechanisms.Methods 70 Juvenile male Wistar rats were randomly divided into three groups:(A) control rats that received neither pilocarpine nor triptolide(n=10),(B) rats that received just pilocarpine(n=30),and(C) rats that received pilocarpine and triptolide(n=30).Neuronal death was evaluated by Nissl and FJB staining methods.Glial activation states were analyzed by immunohistochemistry for glial markers,GFAP and IBa-1.Results Histopathological observations showed that lithium chloride-pilocarpine caused significant hippocampal neuronal loss and glial activation compared with the control group.Pre-treatment with TP efficiently reduced lithium chloride-pilocarpine-induced seizure activities,hippocampal neuron death and glial activation.Conclusion TP exerts a neuroprotective role in the attenuation of brain damage after SE,possibly by inhibiting glial activation to resist inflammatory reaction.