Evidence map›Paper›PMID 35670898›Full record

ArticleMolecular neurobiology2022

Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model.

Sanjay, Jae-Ho Shin, Miey Park, Hae-Jeung Lee

Erratum issuedOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 76 citations in OpenAlex.

  1. Extract fromNutrients · 2024
    Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. 2-aminobutyrate mediates the impact of air pollution on blood biomarkers of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

SanjayDepartment of Food Science and Biotechnology, College of BioNano Technology, Gachon University, Seongnam-si 13120, Gyeonggi-do, Korea.ORCID http://orcid.org/0000-0003-4571-515X
Jae-Ho ShinDepartment of Biomedical Laboratory Science, Eulji University, Gyeonggi-do 461-713, Seongnam-si, Republic of Korea.ORCID http://orcid.org/0000-0002-2141-1090
Miey ParkDepartment of Food and Nutrition, College of BioNano Technology, Gachon University, Seongnam-si 13120, Gyeonggi-do, Korea. mpark@gachon.ac.kr.ORCID http://orcid.org/0000-0002-9124-0004
Hae-Jeung LeeDepartment of Food and Nutrition, College of BioNano Technology, Gachon University, Seongnam-si 13120, Gyeonggi-do, Korea. skysea@gachon.ac.kr.ORCID http://orcid.org/0000-0001-8353-3619
Gachon University · KREulji University · KR

Funding

Cooperative Research Program of the Center for Companion Animal Research Project No. PJ01476703Gachon University research fund of 2022 GCU-202008490009
6 · The paper itself

Abstract

Microglial polarization plays an essential role in the progression and regression of neurodegenerative disorders. Cyanidin-3-O-glucoside (C3G), a dietary anthocyanin found in many fruits and vegetables, has been reported as an antioxidant, anti-inflammatory, and antitumor agent. However, there have been no reports on whether C3G can regulate the M1/M2 shift in an Alzheimer's disease model. We attempted to investigate the effects of C3G on M1/M2 polarization and the mechanism to regulate anti-inflammation and phagocytosis, both in vitro and in vivo. HMC3 cells were treated with β-amyloid (Aβ42) in the presence or absence of 50 μM C3G for different time intervals, and APPswe/PS1ΔE9 mice were orally administered 30 mg/kg/day of C3G for 38 weeks. The in vitro data revealed that C3G could shift the M1 phenotype of microglia to M2 by reducing the expression of M1-specific markers (CD86 and CD80), inflammatory cytokines (IL-Iβ, IL-6, TNF-α), reactive oxygen species, and enhancing the expression of M2-specific markers (CD206 and CD163). The APPswe/PS1ΔE9 mice results were consistent with the in vitro data, indicating a significant reduction in inflammatory cytokines and higher expression of M2-specific markers such as CD206 and Arg1 in C3G-treated Alzheimer's disease model mice. Additionally, C3G was found to upregulate PPARγ expression levels both in vitro and in vivo, whereas a PPARγ antagonist (GW9662) was found to block C3G-mediated effects in vitro. In this study, we confirmed that C3G could regulate microglial polarization by activating PPARγ and eliminating accumulated β-amyloid by enhancing Aβ42 phagocytosis through the upregulation of TREM2.

Indexed as

Alzheimer DiseaseMicrogliaAmyloid beta-PeptidesAnimalsAnthocyaninsCytokinesGlucosidesMembrane GlycoproteinsMicePeptide FragmentsPhagocytosisPPAR gammaReceptors, ImmunologicSignal TransductionAmyloid beta-Peptidesamyloid beta-protein (1-42)AnthocyaninscyanidinCytokinesGlucosidesMembrane GlycoproteinsPeptide FragmentsPPAR gammaReceptors, ImmunologicTrem2 protein, mouseAlzheimer’s diseaseAnthocyaninAnti-inflammationCyanidin-3-O-glucosideM1/M2 shiftNeuroinflammation

Identifiers

PMID35670898
PMCPMC9363298
OpenAlexW4281801389

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.