银杏内酯J对β-淀粉样蛋白诱导的异常突触功能和细胞死亡的保护作用。
Protection against beta-amyloid induced abnormal synaptic function and cell death by Ginkgolide J.
作者信息
Vitolo Ottavio, Gong Bing, Cao Zixuan, Ishii Hideki, Jaracz Stanislav, Nakanishi Koji, Arancio Ottavio, Dzyuba Sergei V, Lefort Roger, Shelanski Michael
机构信息
Department of Pathology and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
出版信息
Neurobiol Aging. 2009 Feb;30(2):257-65. doi: 10.1016/j.neurobiolaging.2007.05.025. Epub 2007 Jul 20.
Abstract
A new Ginkgo biloba extract P8A (TTL), 70% enriched with terpene trilactones, prevents A beta(1-42) induced inhibition of long-term potentiation in the CA1 region of mouse hippocampal slices. This neuroprotective effect is attributed in large part to ginkgolide J that completely replicates the effect of the extract. Ginkgolide J is also capable of inhibiting cell death of rodent hippocampal neurons caused by A beta(1-42). This beneficial and multi-faceted mode of action of the ginkgolide makes it a new and promising lead in designing therapies against Alzheimer's disease.
摘要
一种新的银杏叶提取物P8A（TTL），富含70%的萜类三内酯，可预防β淀粉样蛋白（1-42）诱导的小鼠海马切片CA1区长期增强效应的抑制。这种神经保护作用在很大程度上归因于银杏内酯J，它完全复制了提取物的作用效果。银杏内酯J还能够抑制由β淀粉样蛋白（1-42）引起的啮齿动物海马神经元细胞死亡。银杏内酯这种有益且多方面的作用模式使其成为设计抗阿尔茨海默病疗法的一种新的、有前景的先导物。
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