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作 者:孙晶[1] 孙长凯[2] 范明[3] 丁爱石[3] 尹琳 邬伟[1] 王小同[1]
机构地区:[1]温州医学院附属第二医院神经内科 [2]大连医科大学脑疾病研究所 [3]军事医学科学院基础医学研究所神经生物研究室,北京100850 [4]浙江大连医学大学附属第二医院神经内科
出 处:《中国临床药理学与治疗学》2006年第1期95-98,共4页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:国家自然科学基金项目(№30070267);中国博士后科学基金项目(2001);辽宁省重点科技攻关项目(№2001226005)
摘 要:目的:观察新银杏叶提取物(nGBE)在不同给药模式下对谷氨酸所致海马神经元毒性作用的影响。方法:采用CO2超临界萃取的方法制备nGBE,建立新生Wistar大鼠原代培养的海马神经元谷氨酸毒性模型,采用台盼蓝染色、程序性细胞死亡检测技术及乳酸脱氢酶测定的方法,观察预处理与急救两种给药模型下nGBE的神经保护作用,并与MK-801急性给药相比较。结果:nGBE在两种给药模式下均能不同程度地提高细胞存活率,降低凋亡率,减少LDH漏出量。其中预处理的效果明显优于急救给药处理,但均弱于MK-801组。结论:银杏叶制剂按其现有的临床给药途径即用于脑血管病的急救治疗,就其抗兴奋毒性机制而言,作用较弱,但如果我们将其用于高危人群的预防干预可能有更大价值。AIM: To investigate protective effects of novel extract of Ginkgo biloba (nGBE) in different administration modes on glutamate-induced neuronal damage. METHODS: The values of Essential nGBE were obtained by supercritical CO2 fluid extraction. Based on glutamate excitotoxicity of primary cultures from neonatal Wistar rats hippocampal, by use of Trypan blue dye staining, testing the lactate dehydrogenase leakage from cultured neurons and terminal deoxynucleotidyl transferase- mediated nick end labeling (TUNEL) method, we examined glutamate-induced necrosis and apoptosis. The protective effects of nGBE in different administration modes (pre-treatment and post-treatment) were adopted and compared with the NMDA receptor uncompetitive antagonist MK-801 in acute-treatment. RESULTS: Treatment with nGBE in two administration modes all could increase ratio of surviving neuron, decrease LDH efflux and reduce ratio of neuron apoptosis in different degree, and the benefit of pre-treatment was superior to post-treatment, but inferior to MK-801. CONCLUSION: The extracts of Ginkgo biloba used nowadays in cerebrovascular disease as post-treatment have no prominent effect as far as their mechanism of antiexcitotoxicity. However they may have more value if they were used for precautionary intervention in high-risk population.
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