【摘要】 目的:探讨绞股蓝皂甙(gypenoside,GP)对谷氨酸(glutamate熏Glu)介导的氧化性神经毒性的拮抗作用。方法:体外培养胎鼠大脑皮层神经细胞,建立Glu氧化性损伤模型,用MTT法测定细胞活力,透射电镜观察Glu所致的神经细胞死亡方式,流式细胞术分析细胞凋亡率。结果:GP以时间依赖性方式明显拮抗谷氨酸介导的氧化性神经毒性,于Glu损伤前达到最佳保护效果,Glu氧化性毒性导致神经细胞发生凋亡兼具坏死特征的死亡,Glu损伤组细胞凋亡率(21.63%)明显高于正常对照组(0.09%)及GP保护组(8.94%)。结论:GP可明显拮抗Glu介导的氧化性神经毒性。更多还原

【Abstract】 Objective: To study the protective effects of gypenoside(GP) against oxidative neurotoxicity induced by glutamate. Methods: Primary cortical neurons were prepared from embryonic day 13.5～14 Wistar rats. The oxidative neurotoxicity model was obtained by applying high dosage glutamate. The viability of cells after various treatments was determined by using the method of 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide reduction. The death style of neurons was assayed through transmission electron microscope, and flow cytometry was applied to check the difference of cell apoptosis ratios. Results: GP significantly attenuated glutamate-induced neurotoxicity in primary cultured cortical neurons with a time-dependent manner. The optimal cell viability was obtained by a pre-treatment with GP. Through transmission electron microscope we found that oxidative stress exerted by glutamate induced a form of programmed cell death with characteristics of both apoptosis and necrosis in primary cultured neurons. Flow cytometry analysis showed the apoptosis ratio of glutamate-intoxicated cells (21.63%)was apparently higher than those in both untreated control (0.09%) and the GP-treated cells(8.94%). Conclusion: These results suggest that GP exerts significant neuroprotective effects on cultured cortical cells. Therefore, GP may be efficacious in protecting neurons from oxidative damage produced by exposure to excess glutamate.更多还原