Evidence map›Paper›PMID 36646447›Full record

ArticleBiomolecules & therapeutics2023

A Neuroprotective Action of Quercetin and Apigenin through Inhibiting Aggregation of Aβ and Activation of TRKB Signaling in a Cellular Experiment.

Ya-Jen Chiu, Yu-Shan Teng, Chiung-Mei Chen, Ying-Chieh Sun, Hsiu Mei Hsieh-Li, Kuo-Hsuan Chang, Guey-Jen Lee-Chen

Open access · hybridAbstract read
In one paragraph

Article in Biomolecules & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.0field-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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  10. Evaluation of the In Vitro Blood-Brain Barrier Transport ofInternational journal of molecular sciences · 2025
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  13. Review
  14. Neuroprotective Effect of Naturally Occurring Flavonoids.Central nervous system agents in medicinal chemistry · 2025
    Review
  15. Article
  16. Chemical Characterization and Assessment of the Neuroprotective Potential ofInternational journal of molecular sciences · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Ya-Jen ChiuSchool of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
Yu-Shan TengSchool of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
Chiung-Mei ChenDepartment of Neurology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan 33378, Taiwan.
Ying-Chieh SunDepartment of Chemistry, National Taiwan Normal University, Taipei 11677, Taiwan.
Hsiu Mei Hsieh-LiSchool of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
Kuo-Hsuan ChangDepartment of Neurology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan 33378, Taiwan.
Guey-Jen Lee-ChenSchool of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
National Taiwan Normal University · TWChang Gung Memorial Hospital · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease with progressive memory loss and the cognitive decline. AD is mainly caused by abnormal accumulation of misfolded amyloid β (Aβ), which leads to neurodegeneration via a number of possible mechanisms such as down-regulation of brain-derived neurotrophic factor-tropomyosin-related kinase B (BDNF-TRKB) signaling pathway. 7 ,8-Dihydroxyflavone (7,8-DHF), a TRKB agonist, has demonstrated potential to enhance BDNF-TRKB pathway in various neurodegenerative diseases. To expand the capacity of flavones as TRKB agonists, two natural flavones quercetin and apigenin, were evaluated. With tryptophan fluorescence quenching assay, we illustrated the direct interaction between quercetin/apigenin and TRKB extracellular domain. Employing Aβ folding reporter SH-SY5Y cells, we showed that quercetin and apigenin reduced Aβ-aggregation, oxidative stress, caspase-1 and acetylcholinesterase activities, as well as improved the neurite outgrowth. Treatments with quercetin and apigenin increased TRKB Tyr516 and Tyr817 and downstream cAMP-response-element binding protein (CREB) Ser133 to activate transcription of BDNF and BCL2 apoptosis regulator (BCL2), as well as reduced the expression of pro-apoptotic BCL2 associated X protein (BAX). Knockdown of TRKB counteracted the improvement of neurite outgrowth by quercetin and apigenin. Our results demonstrate that quercetin and apigenin are to work likely as a direct agonist on TRKB for their neuroprotective action, strengthening the therapeutic potential of quercetin and apigenin in treating AD.

Indexed as

AD therapeuticsApigeninAβ cell modelQuercetinTRKB agonistsTryptophan fluorescence quenching assay

Identifiers

PMID36646447
PMCPMC10129860
OpenAlexW4316591935

What OpenQuestion holds

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Registered trials

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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.