Khongsombat Onrawee, Nakdook Walika, Ingkaninan Kornkanok
Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok 65000, Thailand.
Center of Excellence in Medical Biotechnology, Naresuan University, Phitsanulok 65000, Thailand.
J Tradit Complement Med. 2017 Jun 16;8(1):184-189. doi: 10.1016/j.jtcme.2017.05.009. eCollection 2018 Jan.
In Alzheimer's disease, there are numerous amyloid plaques, neurofibrillary tangles, and neuronal loss in several brain areas. Oxidative stress is involved in the mechanisms of Aβ-peptide induced neurotoxicity by the generation of free radical oxidative stress that may lead to neurodegeneration. has various medical properties in Thai folklore medicine including prevent forgetfulness or improve memory. The present study aimed to investigate the effects of root extract (TDE) on Aβ peptides induced neuronal loss and oxidative stress in mice. Male ICR mice were administered with vehicle or TDE (250, 500, and 1000 mg/kg b.w., p.o.) for 28 consecutive days. Then, these mice were given a single intracerebroventricular (i.c.v.) injection of Aβ or phosphate buffer saline (PBS) (10 μg/mouse). The novel object recognition (NOR) test was used to determine memory disturbance. In addition, the neuronal cells in the cerebral cortex and hippocampus were measured by using crystal violet staining and lipid peroxidation was determined by measuring the formation of thiobarbituric acid reactive substances. An i.c.v. injection of Aβ peptides could significantly induce memory impairment, increase level of lipid peroxidation including the neuronal loss in CA3 of hippocampus. However, the mice pretreated with TDE could prevent the memory loss, neuronal loss and decrease lipid peroxidation. These results suggest the potential therapeutic value in dementia of TDE through its antioxidant property.
在阿尔茨海默病中，多个脑区存在大量淀粉样斑块、神经原纤维缠结和神经元丢失。氧化应激通过产生可能导致神经退行性变的自由基氧化应激参与β-淀粉样肽（Aβ）诱导的神经毒性机制。[某种物质]在泰国民间医学中有多种医学特性，包括预防健忘或改善记忆。本研究旨在探讨[某种植物]根提取物（TDE）对Aβ肽诱导的小鼠神经元丢失和氧化应激的影响。雄性ICR小鼠连续28天给予溶剂或TDE（250、500和1000 mg/kg体重，口服）。然后，给这些小鼠单次脑室内（i.c.v.）注射Aβ或磷酸盐缓冲盐水（PBS）（10μg/小鼠）。采用新物体识别（NOR）试验来确定记忆障碍。此外，通过结晶紫染色测量大脑皮质和海马中的神经元细胞，并通过测量硫代巴比妥酸反应性物质的形成来确定脂质过氧化。脑室内注射Aβ肽可显著诱导记忆损伤，增加脂质过氧化水平，包括海马CA3区的神经元丢失。然而，用TDE预处理的小鼠可预防记忆丧失、神经元丢失并减少脂质过氧化。这些结果表明TDE通过其抗氧化特性在痴呆治疗中具有潜在的治疗价值。
