中文摘要：

目的：研究银杏叶提取物（ginkgo biloba extract，GBE）抗兴奋毒性作用及其与胆固醇途径相关性。方法：建立谷氨酸（glutamate，Glu）兴奋毒性模型，设立GBE预处理组、辛伐他汀预处理组、MK-801组，胆固醇预处理组，及GBE＋胆固醇预处理组。通过台盼蓝染色和测定上清中的LDH释放量来判断细胞的损伤程度，利用高效液相色谱检测细胞内胆固醇含量。结果：GBE预处理使暴露于Glu的神经元存活率显著增加（P〈0.01），LDH的释放量显著减少（P〈0.01）。胆固醇预处理加重Glu介导细胞损伤（P〈0．05），GBE＋胆固醇预处理可部分抵消其作用（P〈0.01）；胆固醇预处理可增加细胞内胆固醇含量至（102．38±1．25）μg／mg蛋白，与Glu损伤组比，有显著性提高（P〈0．05）；GBE预处理组细胞内胆固醇含量（64．98±6．14）μg／mg蛋白，GBE＋胆固醇预处理组合量为（76．08±3．04）μg／mg蛋白，两组细胞内胆固醇含量与Glu损伤组相比显著降低（P〈0.05）。结论：GBE预处理给药有显著的抗Glu兴奋毒性的作用，可能与降低细胞内胆固醇相关。

英文摘要：

Objective：To evaluate protective effects of ginkgo biloba extract （GBE） on hippocampal neurons in excitotoxicity system model and its meehanisms. Methods：Glutamate（Glu） excitotoxicity system model of primary hippocampal neurons was edtablished, the experiments included GBE pretreatment group, cholesterol pretreatment group, GBEq-chlolesterol（Cho） pretreatment group, simvastatin（SIM） pretreatment group, MK-801 group and Cho pretreatment group. The degree of neuron damage was evaluated by Trypan blue drying and detection of LDH efflux in supernatant, intracellular cholesterol was detected by high performance liquid chromatography. Results： Comparing with the Glu group, GBE pretreatment group increased cell viability and decreased LDH efflux significantly（P〈0.01）, The Cho pretreatment could aggravate the damage to neurons exposed to Glu （P〈0.05）, GBE＋cholsterol pretreatment could alleviate this injury （P〈0.01）. Cholesterol pretreatment elevated significantly the Intracellular cholesterol to （102.38±1.25）μg/mg compared to Glu group（P〈0.05）, while GBE pretreatment decreased the level of intracellular cholesterol to （64. 98±6. 14）μg/mg protein, comparing the two groups, the difference is significant（P〈0.01 ） intracellular cholesterol of GBE ＋ cholesterol pretreatment group was （76.08±3.04）μg/mg protein which suggested that GBE could decrease intracellular cholesterol in neurons. Conclusion ：GBE pretreament has protective effect on excitototic injury of hippacampal neurons, which is related to the regulation of cholesterol homeostasis in neurons.