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Protective effects of ginsenoside Rg2 against memory impairment and neuronal death induced by Aβ25-35 in rats.

Authors
  • Cui, Jing1
  • Shan, Rui2
  • Cao, Yanqi2
  • Zhou, Yifa3
  • Liu, Chunming4
  • Fan, Yuying5
  • 1 Central Laboratory, Changchun Normal University, Changchun Jilin, 130032, PR China; School of Life Sciences, Northeast Normal University, Changchun Jilin, 130024, PR China. , (China)
  • 2 Central Laboratory, Changchun Normal University, Changchun Jilin, 130032, PR China. , (China)
  • 3 School of Life Sciences, Northeast Normal University, Changchun Jilin, 130024, PR China. , (China)
  • 4 Central Laboratory, Changchun Normal University, Changchun Jilin, 130032, PR China. Electronic address: [email protected] , (China)
  • 5 School of Life Sciences, Northeast Normal University, Changchun Jilin, 130024, PR China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Journal of ethnopharmacology
Publication Date
Feb 10, 2021
Volume
266
Pages
113466–113466
Identifiers
DOI: 10.1016/j.jep.2020.113466
PMID: 33049344
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Ginsenoside Rg2 is an important ingredient of Panax ginseng which often appears in ancient prescriptions for forgetfulness. Ginsenoside Rg2 exert neuroprotective effects and could be a new potential medicine to treat AD. In our previous study, we reported that ginsenoside Rg2 appears protect PC12 cells against Amyloid β-fragment (25-35) (Aβ25-35)-induced apoptosis via the PI3K/Akt pathway. However, there are no in vivo studies on the protective effects of ginsenoside Rg2 on Aβ-induced neurotoxicity. The present study was performed to investigate the protective effects of ginsenoside Rg2 against Aβ25-35-induced memory impairment, and its underlying mechanisms in rats. An Alzheimer's Disease (AD) rat model was established by injecting the rats with Aβ25-35 (1 μg/μl). Cognitive performance was evaluated by the Morris Water Maze test (MWM). The brain sections were processed and neuronal apoptosis in the hippocampus was evaluated by Hematoxylin and Eosin staining (H&E). To explore the anti-neuronal apoptosis mechanism of ginsenoside Rg2, we analyzed the protein expression of Bcl-2/Bax, caspase-3, and phospho-protein kinase B/protein kinase B (p-Akt/Akt) via western blot. A significant improvement in cognitive function was observed in administrated ginsenoside Rg2 AD rats. The histological injury in hippocampus CA1 induced by Aβ25-35 was inhibited following administration of the ginsenoside Rg2. Ginsenoside Rg2 increase the Bcl-2/Bax ratio, attenuate the cleavage of caspase-3, and enhance the phosphorylation of Akt. These findings suggest that ginsenoside Rg2 could ameliorate Aβ25-35-induced cognitive dysfunction by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Copyright © 2020 Elsevier B.V. All rights reserved.

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