一氧化氮在缺氧复氧所致神经细胞凋亡中的作用及银杏叶提取物的保护效应  

Effect of Nitric Oxide on the Cotical Neurons Apoptosis Induced by Hypoxia/ Reoxygenation and EGB Protection

作　　者：季凤清[1] 孙海梅[1] 岳旭[1] 郭艳茹[2] 杜晓宇[1] 郭崇洁 赵天德[2] 

机构地区：[1]首都医科大学组织胚胎学教研室 [2]中日友好临床医学研究所

出　　处：《首都医科大学学报》2001年第3期193-198,共6页Journal of Capital Medical University

基　　金：北京市科干局优秀青年培养基金

摘　　要：为探讨银杏叶提取物对缺氧复氧神经细胞凋亡中一氧化氮 (NO)动态表达的作用 ,对大鼠大脑皮质神经细胞原代分离培养 ,用原位末端标记法 (TUNEL)及流式细胞术检测细胞凋亡 ,用荧光分光光度法检测细胞培养上清液中亚硝酸根含量的变化。结果 :缺氧复氧致胎鼠大脑皮质神经细胞凋亡中NO含量呈双时相增高 (单纯缺氧 2h及缺氧 18h复氧 18h) ,银杏叶提取物 (EGB)对此双时相的NO升高有抑制作用 ,氨基胍 (AG)可抑制缺氧 8h复氧 18h组的NO升高 ,对缺氧 2h组的NO升高无抑制作用。提示 :NO参与了缺氧复氧过程中神经细胞凋亡 ,银杏叶提取物对缺氧复氧神经细胞凋亡有保护作用 ,其作用可能是通过抑制NO而实现的。To explore the effect of extract ginkgo biloba (EGB) on the dynamic expression of nitric oxide (NO) in the neuron apoptosis following hypoxia/reoxygenation(H/R), cerebral neurons of fetal Wistar rats were primarily isolated and cultured. Apoptosis of cultured cerebral cortical neurons following H/R was detected with Tunel and Flow cytometry method. The dynamic changes of NO metabolite nitrite (NO 2 -) in the supernatent solution of cultured neurons were measured by fluorospectrophotometry. No content in the apoptosis of cerebral neurons of fetal Wistar rats increased at H 2R 0 and H 18 R 18 respectively to the normal control group. EGB showed an inhibition function to the increase of NO. AG inhibited the increase of NO at H 8R 18 , but showed no effect on the NO in H 2R 0 group. NO plays a role in the apoptosis of neurons following H/R, and EGB has a protective function on the apoptosis . The probable mechanism of EGB protection is its inhibition of NO.

关 键 词：一氧化氮 缺氧复氧 神经细胞凋亡 银杏叶提取物 保护效应 

分 类 号：R322.81[医药卫生—人体解剖和组织胚胎学]