Characterization of anti-neurodegenerative effects of Polygala tenuifolia in Aβ(25-35)-treated cortical neurons
Characterization of anti-neurodegenerative effects of Polygala tenuifolia in Aβ(25-35)-treated cortical neurons
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DOI：
10.1248/bpb.29.1892
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发表时间：
2006-09-01
影响因子：
2
通讯作者：
Tohda, Chihiro
中科院分区：
文献类型：
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作者：
Naito, Rie;Tohda, Chihiro
尽管在中国和日本传统医学中，远志（Polygala tenuifolia WILLD，PT）被经典地提及为抗痴呆药物，但基础研究表明仅增强胆碱能功能。在阿尔茨海默病中，神经炎性萎缩和突触丢失发生在神经元死亡事件之前，并且可能是记忆障碍的第一个触发因素。因此，我们研究了远志（PT）对A β（25-35）诱导的神经元损伤的影响，使用大鼠皮层神经元来表征PT在A β诱导的神经元损伤下的活性。在A β（25-35）诱导的轴突萎缩后，用PT的水提取物处理可剂量依赖性地增加轴突长度。然而，用PT提取物处理不能恢复由A β（25-35）诱导的树突萎缩和突触丢失。相比之下，PT提取物完全抑制A β（25-35）诱导的细胞损伤。通过表征PT对神经元形态可塑性和细胞损伤的影响，澄清了PT作为抗痴呆药物的有用性和不足。
Although Polygala tenuifolia WILLD (PT) was classically mentioned as an anti-dementia drug in Chinese and Japanese traditional medicine, basic research showed only enhancement of the cholinergic function. In Alzheimer's disease, neuritic atrophy and synaptic loss occur prior to neuronal death event, and may be the first trigger of the memory impairment. Therefore, we studied effects of Polygala tenuifolia WILLD (PT) on A beta(25-35)-induced neuronal damage using rat cortical neurons for characterization of activities of PT under Aft-induced neuronal damage. Treatment with the water extract of PT enhanced axonal length dose-dependently after A beta(25-35)-induced axonal atrophy. However, dendritic atrophy and synaptic loss induced by A beta(25-35) were not recovered by treatment with PT extract. In contrast, A beta(25-35)-induced cell damage was completely inhibited by PT extract. By characterization of PT effects on neuronal morphological plasticity and cell damage, usefulness as well as an insufficiency of PT as an anti-dementia drug was clarified.