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作 者:顾承志[1] 黄国祥[1] 黄志东[1] 黄怀宇[1]
机构地区:[1]南通大学第二附属医院神经内科,南通226001
出 处:《药学与临床研究》2009年第6期439-442,共4页Pharmaceutical and Clinical Research
摘 要:目的:探究银杏叶提取物(EGb)对谷氨酸诱导体外培养神经细胞损伤的保护作用及相关机制,为EGb应用于缺血性卒中提供依据。方法:取孕15~18天SD胎鼠的皮层神经细胞进行原代培养(对照组),在此基础上,建立谷氨酸诱导神经细胞损伤模型(Glu组)。向Glu组中预先加入4种不同浓度(12.5~100mg.L-1)EGb作用(研究组)。通过测定神经细胞NO及LDH的释放量来反映神经细胞损伤程度。结果:谷氨酸呈浓度依赖性升高神经细胞NO及LDH释放量;与Glu组相比较,EGb(12.5~100mg.L-1)能不同程度的抑制NO、LDH释放,且EGb浓度为50mg.L-1时作用最显著(P<0.01)。结论:谷氨酸通过NO诱导神经细胞损伤,EGb通过抑制NO、LDH释放实现拮抗谷氨酸神经细胞毒性作用。Objective: To explore the protective effect of Ginkgo biloba extract (EGb) against glutamate (Glu) induced injuries on cortical neurons in vitro and the mechansim basis of EGb in the treatment of patients with ischemia stroke. Methods: Cortical neurons were removed from 15-18-day SD- rat fetuses aseptically and primary cultivated (control group). The injury model of neurons was formed by giving glutamate ( Glu group ) ; the Glu groups pretreated with different concentrations of EGb (12.5 -100 mg·L^-1)were taken as EGb groups. The effects of EGb on Glu injury in neurons were evaluated by the level of NO and LDH in the nutrient solution of cultured neurons. Results: Glu could dose dependently increase the levels of NO and LDH in cortical neurons. Compared with the Glu group, EGb (12.5 -100 mg·L^-1) could decrease the levels of NO and LDH in the nutrient solution of cultured neurons significantly when the concentration was 50 mg·L^-1 (P 〈 0.01 ). Conclusions : The injury of cortex neurons induced by Glu was mediated by NO and LDIt. EGb plays a protective role in Glu induced neuron injury via inhibiting the release of NO and LDH.
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