银杏内酯B对谷氨酸诱发原代培养皮层神经元损伤的实验研究  

An Experimental Study Of Ginkgobalide B On Primary Cultured Cortical Neuron Damaged by Glutamic Acid

作　　者：梅世昌[1] 张硕峰[2] 黄贱英[2] 孙建宁[2] 

机构地区：[1]解放军总医院科技开发中心,北京10085 [2]北京中医药大学,北京100102

出　　处：《解放军药学学报》2008年第2期107-109,共3页Pharmaceutical Journal of Chinese People's Liberation Army

摘　　要：目的观察银杏内酯B(Ginkgobalide B,GB)对谷氨酸致原代培养皮层神经元损伤的保护作用。方法采用体外培养皮层神经元的方法,利用终浓度为0.5mmol·L-1的谷氨酸造成皮层神经元损伤,通过测定细胞存活率、细胞活性、乳酸脱氢酶(LDH)漏出率、丙二醛(MDA)含量,超氧化物歧化酶(SOD)活性,研究GB对谷氨酸造成神经元损伤的保护作用机制。结果GB10-5mo·lL-1可抑制谷氨酸所致LDH漏出率的升高。GB10-4、10-5mol·L-1可提高神经细胞活性;扭转谷氨酸致神经细胞存活率的下降;升高SOD酶的活性,抑制谷氨酸所致MDA含量的升高。结论提示GB对谷氨酸所致原代皮层神经元的损伤具有保护作用。Aim To study the protective effect of Ginkgobalide B （GB） on neuron damaged by 0.5mmol·L^-1 glutamic acid. Methods The results were determined by the LDH leakage rate, survival rate, activity of neurons SOD activity, MDA content, GSH content, and NO content in culture fluid collected after lesion of glutamic acid. Results GB 10^-5mol·L^-1 can inhibit the increase of the LDH leakage rate caused by the lesion of glutamic acid. GB 10^-4,10^-5mol·L^-1 can increase the survival rate and activity of neurons, the activity of SOD,the content of while decreasing the content of MDA. Conclusion The results implicated that GB protected neuron lesioned by glutamic acid.

关 键 词：银杏内酯B 谷氨酸 

分 类 号：R965[医药卫生—药理学]