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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 6473506, 17 pages
Research Article

Ginsenoside Rg1 Ameliorates Behavioral Abnormalities and Modulates the Hippocampal Proteomic Change in Triple Transgenic Mice of Alzheimer’s Disease

1Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China
2Department of Obstetrics, Shenzhen People’s Hospital, The Second Clinical Medical College of Jinan University, Shenzhen 518020, China
3Department of Histology and Embryology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
4Institute of New Drug Research and Guangzhou Key Laboratory of Innovative Chemical Drug Research in Cardio-cerebrovascular Diseases, Jinan University College of Pharmacy, Guangzhou 510632, China
5Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430070, China
6School of Pharmacy, Health Science Center, Shenzhen University, Shenzhen 518055, China

Correspondence should be addressed to Xifei Yang; moc.liamg@gnayiefix

Received 15 May 2017; Revised 7 August 2017; Accepted 24 August 2017; Published 24 October 2017

Academic Editor: Juan M. Zolezzi

Copyright © 2017 Lulin Nie et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, so far, there are no effective measures to prevent and cure this deadly condition. Ginsenoside Rg1 (Rg1) was shown to improve behavioral abnormalities in AD; however, the potential mechanisms remain unclear. In this study, we pretreated 7-month-old 3xTg-AD mice for 6 weeks with Rg1 and evaluated the effects of Rg1 on the behaviors and the protein expression of hippocampal tissues. The behavioral tests showed that Rg1 could improve the memory impairment and ameliorate the depression-like behaviors of 3xTg-AD mice. Proteomic results revealed a total of 28 differentially expressed hippocampal proteins between Rg1-treated and nontreated 3xTg-AD mice. Among these proteins, complexin-2 (CPLX2), synapsin-2 (SYN2), and synaptosomal-associated protein 25 (SNP25) were significantly downregulated in the hippocampus of 3xTg-AD mice compared with the WT mice, and the treatment of Rg1 modulated the expression of CPLX2 and SNP25 in the hippocampus of 3xTg-AD mice. The expression of CPLX2, SYN2, and SNP25 was further validated by Western blot analysis. Taken together, we concluded that Rg1 could be a potential candidate drug to improve the behavioral deficits in AD via modulating the expression of the proteins (i.e., CPLX2, SYN2, and SNP25).