Cited by 36Alzheimer's disease research and treatmentsMedicinal Plants and NeuroprotectionDementia and Cognitive Impairment Research

Cyanidin 3- O -β-glucopyranoside activates peroxisome proliferator-activated receptor-γ and alleviates cognitive impairment in the APP swe /PS1 ΔE9 mouse model

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Song, Nan, Zhang, Ling, Chen, Wei, Zhu, Hua, Deng, Wei, Han, Yunlin, Guo, Jianguo, Qin, Chuan·2016·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

Alzheimer's disease (AD) is currently one of the most common neurodegenerative disorders worldwide. To date, no cure has been developed for AD, and some disease-modifying treatments show side effects and low efficacy. Increasing evidence shows that cyanidin 3-O-β-glucopyranoside (Cy3G), which is naturally derived from many plants, may provide protection against neurodegenerative diseases including AD; however, its exact role is still unclear. Therefore, we investigated the mechanisms of the effects of Cy3G on beta-amyloid 25-35 (Aβ25-35)-induced SH-SY5Y cell injury and cognitive impairment in the APP(swe)/PS1(ΔE9) (PAP) mouse model of AD. Furthermore, we aimed to determine the molecular target initiated by Cy3G. The data indicated that Cy3G-mediated neuroprotection involved the inhibition of Aβ25-35 binding to the cell surface and spontaneous aggregation of Aβ25-35 fibrils at the molecular level. Furthermore, in an in vitro study, Aβ25-35-mediated cytotoxicity, which was caused by inducing apoptotic cell death and ROS formation, was also ameliorated by Cy3G intervention. In addition, upregulation of peroxisome proliferator-activated receptor-γ (PPARγ) protein involved in glucose/lipid metabolism by Cy3G treatment verified that the initiated molecule was Cy3G. In an in vivo study, Cy3G was shown to alleviate cognitive impairment, improve cerebral glucose uptake and decrease fasting blood glucose levels. In conclusion, Cy3G ameliorates amyloid β peptide-induced injury both in vitro and in vivo through the PPARγ pathway. Thus, Cy3G has a good safety profile as a potential natural PPARγ agonist and may be used as an ideal alternative to traditional disease-modifying treatments against AD.

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  • Treatments with either total anthocyanins extracted from bilberry and black currant or isolated cyanidin-3-O-glucopyranoside were able to ameliorate cognitive functions in APP/PS1 mice.

    “Treatments with either total anthocyanins extracted from bilberry and black currant [106] or isolated cyanidin-3-O-glucopyranoside, which is the predominant anthocyanin in colored fruit and vegetables [107], were able to ameliorate cognitive functions in APP/PS1 mice.”

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Authors
Song, N., Zhang, L., Chen, W., Zhu, H., Deng, W., Han, Y., Guo, J., & Qin, C.
Affiliations
Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
Corresponding author
Qin, Chuan
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2016-09
Volume
1862
Issue
9
Pages
1786-1800
ISSN
0925-4439 (ISSN-L)
OpenAlex
W2394714028
Cited by
36
References
66
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 4 · 2018: 2 · 2017: 5
FWCI
2.95
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Science Fund for Young Scholars (81500938)
  • PUMC Youth Fund and Fundamental Research Funds for the Central Universities (3332015151)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
PPARγ, Alzheimer's disease, amyloid beta 25-35, cognitive impairment, neuroprotection, SH-SY5Y cells, apoptosis, reactive oxygen species, brain glucose uptake, anthocyanins
MeSH terms
Alzheimer Disease, Animals, Anthocyanins, Brain, Cell Line, Disease Models, Animal, Female, Glucose, Glucosides, Humans, Male, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, Transgenic, Neurons, Peptide Fragments, Recombinant Fusion Proteins, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Apoptosis, Reactive Oxygen Species, Microscopy, Electron, Transmission, PPAR gamma, Mice, Presenilin-1, Cognitive Dysfunction, Protein Aggregation, Pathological

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