摘要
目的 :观察银杏内酯 (ginkgolide ,Gin)对缺氧诱导的大鼠皮层神经元凋亡的保护作用。方法 :选用胎龄 14～ 16d的SD胎鼠的大脑皮层细胞进行原代培养 ,建立缺氧神经元损伤模型。实验分为药物实验组 (Gin组 )、空白对照组、阳性对照组 (MK 80 1) ,每组均进行有糖和无糖培养两种处理。应用MTT法分析细胞存活率、AnnexinV PE双标流式细胞仪法定量分析细胞早期凋亡。结果 :MTT结果显示 ,Gin使皮层神经元存活率明显增加 ,且有糖的缺氧组皮层神经元存活率优于无糖组 ;流式细胞仪测定结果显示 ,预先加入Gin(终浓度 37 5 μg/ml)的一组神经元的凋亡峰明显低于空白组 ,而无糖处理组凋亡峰均高于有糖处理组。结论 :银杏内酯 (37 5 μg/ml)对缺氧损伤的皮层神经元具有保护作用 ,可拮抗缺氧条件下体外培养的皮层神经元的早期凋亡。
AIM:To observe protective effects of ginkgolide(Gin) of rat cortical neurons from early apoptosis induced by hypoxia.METHOD: Primary culture of E 14-16days fetal rat cortical neurons was used to establish hypoxia injury model. There were three groups: Gin group, blank control group and positive control group. The three groups were also subdivided into two subgroups: hypoxia with glucose (glucose group) and hypoxia without glucose (glucose-free group). The neuronal viability in primary cultures from rat cerebral cortex was assessed using MTT assays. The quality changes of neuronal early apoptosis were measured by flow cytometry (FCM) using Annexin V-PE staining. RESULT:MTT assays indicated that Gin apparently increased viability of cortical neurons and that viability of glucose group is prior to that of glucose-free group. FCM results suggested that the apoptosis number of Gin(ultimate concentration 37.5 μg/ml) group was markedly lower than that of blank group and the apoptosis number of glucose group was higher than that of glucose-free group. CONCLUSION:Gin(37.5 μg/ml) protected rat cortical neurons induced by hypoxia and could antagonise early apoptosis of neurons.
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2003年第5期465-468,共4页
Journal of China Pharmaceutical University
基金
交通部九五通达计划资助项目 (编号 95 0 4 0 3 41)~~
