Naito Rie, Tohda Chihiro
Division of Biofunctional Evaluation, Research Center for Ethnomedicine, Institute of Natural Medicine, University of Toyama, Toyoma, Japan.
Biol Pharm Bull. 2006 Sep;29(9):1892-6. doi: 10.1248/bpb.29.1892.
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 Abeta(25-35)-induced neuronal damage using rat cortical neurons for characterization of activities of PT under Abeta-induced neuronal damage. Treatment with the water extract of PT enhanced axonal length dose-dependently after Abeta(25-35)-induced axonal atrophy. However, dendritic atrophy and synaptic loss induced by Abeta(25-35) were not recovered by treatment with PT extract. In contrast, Abeta(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.
尽管远志在中日传统医学中一直被经典地提及为一种抗痴呆药物，但基础研究表明其仅能增强胆碱能功能。在阿尔茨海默病中，神经突萎缩和突触丧失先于神经元死亡事件发生，并且可能是记忆障碍的首要触发因素。因此，我们使用大鼠皮质神经元研究了远志对β淀粉样蛋白（25-35）诱导的神经元损伤的影响，以表征远志在β淀粉样蛋白诱导的神经元损伤下的活性。在β淀粉样蛋白（25-35）诱导轴突萎缩后，用远志水提取物处理可剂量依赖性地增加轴突长度。然而，用远志提取物处理并不能恢复由β淀粉样蛋白（25-35）诱导的树突萎缩和突触丧失。相反，远志提取物可完全抑制β淀粉样蛋白（25-35）诱导的细胞损伤。通过表征远志对神经元形态可塑性和细胞损伤的影响，阐明了远志作为抗痴呆药物的有效性和不足之处。
