Evidence map›Paper›PMID 34500626›Full record

ArticleMolecules (Basel, Switzerland)2021

Apigenin Ameliorates Scopolamine-Induced Cognitive Dysfunction and Neuronal Damage in Mice.

Yeojin Kim, Jihyun Kim, Meitong He, Ahyoung Lee, Eunju Cho

Abstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Food science & nutrition · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Neuroprotective Potential ofBiomolecules · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Neurotrophic Natural Products.Progress in the chemistry of organic natural products · 2024
    Article
  17. Ranuncoside's attenuation of scopolamine-induced memory impairment in mice via Nrf2 and NF-ĸB signaling.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  18. Article
  19. Article
  20. Animal Models of Cognitive Deficits for Probiotic Treatment.Food science of animal resources · 2022
    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

5 authors.

Yeojin KimDepartment of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Korea.
Jihyun KimDepartment of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Korea.ORCID 0000-0001-8232-2932
Meitong HeDepartment of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Korea.
Ahyoung LeeDepartment of Food Science, Gyeongsang National University, Jinju 52725, Korea.ORCID 0000-0002-3489-7798
Eunju ChoDepartment of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Korea.ORCID 0000-0003-4282-3219

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the protective effect and mechanisms of apigenin against cognitive impairments in a scopolamine-injected mouse model. Our results showed that intraperitoneal (i.p.) injection of scopolamine leads to learning and memory dysfunction, whereas the administration of apigenin (synthetic compound, 100 and 200 mg/kg/day) improved cognitive ability, which was confirmed by behavioral tests such as the T-maze test, novel objective recognition test, and Morris water maze test in mice. In addition, scopolamine-induced lipid peroxidation in the brain was attenuated by administration of apigenin. To further evaluate the protective mechanisms of apigenin on cognitive and memory function, Western blot analysis was carried out. Administration of apigenin decreased the B-cell lymphoma 2-associated X/B-cell lymphoma 2 (Bax/Bcl-2) ratio and suppressed caspase-3 and poly ADP ribose polymerase cleavage. Furthermore, apigenin down-regulated the β-site amyloid precursor protein-cleaving enzyme, along with presenilin 1 (PS1) and PS2 protein levels. Apigenin-administered mice showed lower protein levels of a receptor for advanced glycation end-products, whereas insulin-degrading enzyme, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB) expression were promoted by treatment with apigenin. Therefore, this study demonstrated that apigenin is an active substance that can improve cognitive and memory functions by regulating apoptosis, amyloidogenesis, and BDNF/TrkB signaling pathways.

Indexed as

AnimalsApigeninApoptosisBrainBrain-Derived Neurotrophic FactorCognitive DysfunctionDisease Models, AnimalLipid PeroxidationMemoryMiceNeuronsNeuroprotective AgentsProto-Oncogene Proteins c-bcl-2Receptor, trkBScopolamineSignal TransductionApigeninBrain-Derived Neurotrophic FactorNeuroprotective AgentsProto-Oncogene Proteins c-bcl-2Receptor, trkBScopolamineapigenincognitive abilityneuronal damageoxidative stressscopolamine

Identifiers

PMID34500626
PMCPMC8433809

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.