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探索人参皂苷Rh1在睡眠剥夺诱导的小鼠记忆损伤模型中的作用。

Exploring the Effect of Ginsenoside Rh1 in a Sleep Deprivation-Induced Mouse Memory Impairment Model.

作者信息

Lu Cong, Shi Zhe, Dong Liming, Lv Jingwei, Xu Pan, Li Yinghui, Qu Lina, Liu Xinmin

机构信息

Research Center for Pharmacology and Toxicology, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Hunan University of Chinese Medicine, Changsha, Hunan, China.

出版信息

Phytother Res. 2017 May;31(5):763-770. doi: 10.1002/ptr.5797. Epub 2017 Feb 28.

DOI:10.1002/ptr.5797
PMID:28244162
Abstract

Panax ginseng C.A. Meyer (Araliaceae) has been used in traditional Chinese medicine for enhancing cognition for thousands of years. Ginsenoside Rh1, a constituent of ginseng root, as with other constituents, has memory-improving effects in normal mice and scopolamine-induced amnesic mice. Sleep deprivation (SD) is associated with memory impairment through induction of oxidative stress. The present study investigated the effect of Rh1 against SD-induced cognitive impairment and attempted to define the possible mechanisms involved. Ginsenoside Rh1 (20 μmol/kg; 40 μmol/kg) and modafinil (0.42 g/kg) were administered to the mice intraperitoneally for 23 days. After 14-day SD, locomotor activity was examined using the open field test, and the object location recognition and Morris water maze tests were used to evaluate cognitive ability. The cortex and hippocampus were then dissected and homogenized, and levels and activities of antioxidant defense biomarkers were evaluated to determine the level of oxidative stress. The results revealed that Rh1 prevented cognitive impairment induced by SD, and its ability to reduce oxidative stress in cortex and hippocampus may contribute to the mechanism of action. Copyright © 2017 John Wiley & Sons, Ltd.

摘要

人参(五加科)在传统中药中用于增强认知已有数千年历史。人参皂苷Rh1是人参根的一种成分,与其他成分一样,对正常小鼠和东莨菪碱诱导的失忆小鼠具有改善记忆的作用。睡眠剥夺(SD)通过诱导氧化应激与记忆损伤相关。本研究调查了Rh1对SD诱导的认知损伤的影响,并试图确定其中可能涉及的机制。将人参皂苷Rh1(20μmol/kg;40μmol/kg)和莫达非尼(0.42g/kg)腹腔注射给小鼠,持续23天。在进行14天的SD后,使用旷场试验检测运动活性,并使用物体位置识别和莫里斯水迷宫试验评估认知能力。然后解剖并匀浆大脑皮层和海马体,评估抗氧化防御生物标志物的水平和活性,以确定氧化应激水平。结果显示,Rh1可预防SD诱导的认知损伤,其降低大脑皮层和海马体氧化应激的能力可能是其作用机制。版权所有©2017约翰·威利父子有限公司。

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