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目的 探讨外源性神经节苷脂GM1对癫痫大鼠脑损伤有无保护作用。方法 采用硫代氨基脲 (7.5mg/kg)诱导大鼠癫痫发作模型 ,用免疫组化方法动态观察致痫组大鼠和GM 1干预组大鼠在癫痫发作 2 4小时、4 8小时、72小时及 7天时 ,以及正常对照组、生理盐水组大鼠 72小时时神经生长因子 (NGF)在实验大鼠海马及额叶神经细胞表达情况。同时应用电镜技术观察受损海马神经细胞形态及结构变化。结果 正常对照组和生理盐水组大鼠无癫痫发作 ,致痫组和GM1干预组大鼠有Ⅰ Ⅴ级癫痫发作。免疫组化结果显示 ,癫痫鼠在其海马、额叶有较多的NGF阳性神经细胞表达 ,而未致痫鼠偶有NGF阳性细胞表达 (P <0 .0 5 )。在致痫鼠中 ,GM1干预后NGF表达明显高于未干预组 (P <0 .0 5 ) ,且以 72小时NGF表达为最高(P <0 .0 5 )。电镜显示癫痫鼠神经细胞损伤 ,但GM1干预后损伤减轻 ,而正常对照组和生理盐水组神经细胞形态和结构正常。结论 癫痫发作可引起脑细胞损伤 ;GM1对癫痫大鼠脑损伤具有一定保护作用 ,其保护作用可能通过诱导NGF表达增多来实现。
Objective To investigate whether exogenous ganglioside GM1 can protect brain from epilepsy in rats. Methods Thiosemicarbazide (7.5 mg / kg) was used to induce the seizure model in rats. Immunohistochemistry was used to observe the changes of seizures induced by epilepsy in 24 h, 48 h, 72 h Hour, 7 day, and normal control group, the expression of nerve growth factor (NGF) in the hippocampus and the frontal lobe neurons of the rats in the saline group at 72 hours. At the same time, electron microscopy was used to observe the morphology and structure of damaged hippocampal neurons. Results There was no epileptic seizures in the normal control group and the saline group. The rats in the epileptic group and the GM1 intervention group were grade Ⅰ Ⅴ seizures. The results of immunohistochemistry showed that hippocampus and frontal lobe had more NGF positive neurons in epileptic mice than those in non-epileptic rats (P <0.05). In the epileptic rats, the expression of NGF after GM1 intervention was significantly higher than that of the non-intervention group (P <0.05), and the expression of NGF was the highest at 72 hours (P <0.05). Electron microscope showed neuronal cell damage in epileptic rats, but the injury was relieved after GM1 intervention, while the morphology and structure of neurons in normal control group and normal saline group were normal. Conclusions Epileptic seizures can cause brain cell injury. GM1 may have a protective effect on brain injury induced by epilepsy, and its protective effect may be through the induction of increased NGF expression.