Evidence map›Paper›PMID 24379523›Full record

ArticleMediators of inflammation2013

IRAK1/4-targeted anti-inflammatory action of caffeic acid.

Woo Seok Yang, Deok Jeong, Young-Su Yi, Jae Gwang Park, Hyohyun Seo, Sang Hyun Moh, Sungyoul Hong, Jae Youl Cho

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  18. Frontiers in pharmacology · 2021
    Review
  19. Review
  20. ExogenousPlants (Basel, Switzerland) · 2019
    Article
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

8 authors at 1 institution in 1 country.

Woo Seok YangDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Deok JeongDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Young-Su YiDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Jae Gwang ParkDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Hyohyun SeoAnti-aging Research Institute, BIO-FD&C Co., Ltd, Incheon 406-840, Republic of Korea.
Sang Hyun MohAnti-aging Research Institute, BIO-FD&C Co., Ltd, Incheon 406-840, Republic of Korea.
Sungyoul HongDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Jae Youl ChoDepartment of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Sungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caffeic acid (CA) is a phenolic compound that is frequently present in fruits, grains, and dietary supplements. Although CA has been reported to display various biological activities such as anti-inflammatory, anti-cancer, anti-viral, and anti-oxidative effects, the action mechanism of CA is not yet fully elucidated. In this study, the anti-inflammatory action mechanism of CA was examined in lipopolysaccharide (LPS) treated macrophages (RAW264.7 cells) and HCl/EtOH-induced gastritis. CA was found to diminish nitric oxide (NO) and prostaglandin E2 (PGE2) production in LPS-stimulated RAW264.7 cells. Additionally, mRNA levels of tumor necrosis factor (TNF)-α, cyclooxygenase (COX)-2, and inducible NO synthase (iNOS) were downregulated by CA. CA also strongly suppressed the nuclear translocation of AP-1 family proteins and the related upstream signaling cascade composed of interleukin-1 receptor-associated kinase 1 (IRAK1), IRAK4, TGF-β-activated kinase 1 (TAK1), mitogen-activated protein kinase kinase 4/7 (MKK4/7), and c-Jun N-terminal kinase (JNK). In a direct kinase assay, CA was revealed to directly inhibit IRAK1 and IRAK4. CA also ameliorated HCl/EtOH-induced gastric symptoms via the suppression of JNK, IRAK1, and IRAK4. Therefore, our data strongly suggest that CA acts as an anti-inflammatory drug by directly suppressing IRAK1 and IRAK4.

Indexed as

AnimalsAnti-Inflammatory AgentsCaffeic AcidsCells, CulturedHEK293 CellsHumansInterleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesMaleMiceMice, Inbred ICRNitric Oxide Synthase Type IITranscription Factor AP-1Tumor Necrosis Factor-alphaAnti-Inflammatory Agentscaffeic acidCaffeic AcidsInterleukin-1 Receptor-Associated KinasesJNK Mitogen-Activated Protein KinasesNitric Oxide Synthase Type IITranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID24379523
PMCPMC3863464
OpenAlexW2145584128

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.