Neuroprotective effects of 20(S)-protopanaxatriol (PPT) on scopolamine-induced cognitive deficits in mice

文献类型： 外文期刊

第一作者： Lu, Cong

作者： Lu, Cong;Lv, Jingwei;Dong, Liming;Jiang, Ning;Liu, Xinmin;Lu, Cong;Lv, Jingwei;Dong, Liming;Jiang, Ning;Liu, Xinmin;Lu, Cong;Wang, Yan;Fan, Bei;Wang, Fengzhong;Wang, Qiong;Li, Yinghui;Chen, Shanguang

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关键词： 20(S)-protopanaxatriol (PPT); cholinergic function; cognitive deficits; oxidative stress; scopolamine

期刊名称：PHYTOTHERAPY RESEARCH （ 影响因子：5.878； 五年影响因子：5.286 ）

ISSN： 0951-418X

年卷期： 2018 年 32 卷 6 期

页码：

收录情况： SCI

摘要： 20(S)-protopanaxatriol (PPT), one of the ginsenosides from Panax ginseng, has been reported to have neuroprotective effects and to improve memory. The present study was designed to investigate the protective effect of PPT on scopolamine-induced cognitive deficits in mice. Male Institute of Cancer Research mice were pretreated with 2 different doses of PPT (20 and 40mol/kg) for 27days by intraperitoneal injection, and scopolamine (0.75mg/kg) was injected intraperitoneally for 9days to induce memory impairment. Thirty minutes after the last pretreatment, the locomotor activity was firstly examined to evaluate the motor function of mice. Then, memory-related behaviors were evaluated, and the related mechanism was further researched. It was founded that PPT treatment significantly reversed scopolamine-induced cognitive impairment in the object location recognition experiment, the Morris water maze test, and the passive avoidance task, showing memory-improving effects. PPT also significantly improved cholinergic system reactivity and suppressed oxidative stress, indicated by inhibition of acetylcholinesterase activity, elevation of acetylcholine levels, increasing superoxide dismutase activity and lowering levels of malondialdehyde in the hippocampus. In addition, the expression levels of Egr-1, c-Jun, and cAMP responsive element binding in the hippocampus were significantly elevated by PPT administration. These results suggest that PPT may be a potential drug candidate for the treatment of cognitive deficit in Alzheimer's disease.

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