2. Academic Validation
  3. A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer's disease

A UPLC/MS-based metabolomics investigation of the protective effect of ginsenosides Rg1 and Rg2 in mice with Alzheimer's disease

  • J Ginseng Res. 2016 Jan;40(1):9-17. doi: 10.1016/j.jgr.2015.04.006.
Naijing Li 1,  Ying Liu 2,  Wei Li 2,  Ling Zhou 2,  Qing Li 2,  Xueqing Wang 3,  Ping He 1
Affiliations

Affiliations

  • 1 Department of Gerontology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, China.
  • 2 College of Pharmacy, Shenyang Pharmaceutical University, Shenyang, China.
  • 3 Department of Gastroenterology, The Shengjing Affiliated Hospital, China Medical University, Shenyang, China.
PMID: 26843817 DOI: 10.1016/j.jgr.2015.04.006
Abstract

Background: Alzheimer's disease (AD) is a progressive brain disease, for which there is no effective drug therapy at present. Ginsenoside Rg1 (G-Rg1) and G-Rg2 have been reported to alleviate memory deterioration. However, the mechanism of their anti-AD effect has not yet been clearly elucidated.

Methods: Ultra performance liquid chromatography tandem MS (UPLC/MS)-based metabolomics was used to identify metabolites that are differentially expressed in the brains of AD mice with or without ginsenoside treatment. The cognitive function of mice and pathological changes in the brain were also assessed using the Morris water maze (MWM) and immunohistochemistry, respectively.

Results: The impaired cognitive function and increased hippocampal Aβ deposition in AD mice were ameliorated by G-Rg1 and G-Rg2. In addition, a total of 11 potential biomarkers that are associated with the metabolism of lysophosphatidylcholines (LPCs), hypoxanthine, and sphingolipids were identified in the brains of AD mice and their levels were partly restored after treatment with G-Rg1 and G-Rg2. G-Rg1 and G-Rg2 treatment influenced the levels of hypoxanthine, dihydrosphingosine, hexadecasphinganine, LPC C 16:0, and LPC C 18:0 in AD mice. Additionally, G-Rg1 treatment also influenced the levels of phytosphingosine, LPC C 13:0, LPC C 15:0, LPC C 18:1, and LPC C 18:3 in AD mice.

Conclusion: These results indicate that the improvements in cognitive function and morphological changes produced by G-Rg1 and G-Rg2 treatment are caused by regulation of related brain metabolic pathways. This will extend our understanding of the mechanisms involved in the effects of G-Rg1 and G-Rg2 on AD.

Keywords

Alzheimer's disease; ginseng; ginsenoside Rg1; ginsenoside Rg2; metabolomics.

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