摘要
以 β-淀粉样蛋白2 5 35片段 (β-AmyloidPeptide 2 5 35,β AP2 5 35)诱发原代培养小鼠皮层神经元出现凋亡作为阿尔采末症 (Alzheimer′sDisease ,AD)的离体模型 ,在此基础上观察了银杏叶提取物 (ExtractofleavesofGinkgobilobaL .,EGb76 1)及其主要活性成分内酯B(GinkgolideB ,GinB)对上述神经元损伤的对抗作用 .结果表明 ,EGb76 1能抑制 β AP2 5 35引起的神经元活性的下降和超微结构的改变 ,即抑制 β AP2 5 35诱导的神经元凋亡 ,从而为EGb76 1临床用于防治AD提供了实验依据 .
MTT assay and morphological (including ultrastructural) observation were used to study the protective effects of both extract of leaves of Ginkgo Bioloba L. (EGb761) and its main active component ginkgolide B (Gin B) against β amyloid peptide 25?35 (β AP 25?35 ) induced neuronal apoptosis in cultured cortical neurons. Neurons were dissociated from 13～14 day old fetal mice, cultured in DMEM plus 10% bovine and 10% horse serums for 7 days and insulted by 25?μmol/mL β AP 25?35 , which has been considered as one of the in vitro model of Alzheimer's Disease (AD). Main results are as follows: Only aggregrated β AP 25?35 could decrease neuronal viability and induce typical apoptotic ultrastructural changes in neurons such as blebbing of membrane surface under scanning electron microscopy (SEM) and patches of condensed chromatin lying against nuclear membrane under transmission electron microscopy (TEM). However, both 62.5 μg/mL EGb761 and 37.5 μg/mL Gin B could inhibit 25 μmol/mL β AP 25?35 induced both decrease of neuronal viability and morphological changes. Moreover, neuronal ultrastructural alterations which demonstrated apoptosis produced by aggregrated β AP 25?35 could be blocked by EGb761. These findings provide first evidence for direct protective effects of EGb761 against β AP 25?35 induced neuronal injury and suggest possible clinical use of EGb761 to prevent and cure neurodegenerrative disease, especially AD.
出处
《南京大学学报（自然科学版）》
CSCD
北大核心
2001年第2期223-227,共5页
Journal of Nanjing University（Natural Science）
基金
江苏省自然科学基金(BK9303011)
