Evidence map›Paper›PMID 25541056›Full record

ArticleBMB reports2015

Butein, a tetrahydroxychalcone, suppresses pro-inflammatory responses in HaCaT keratinocytes.

Won Yong Seo, Gi Soo Youn, Soo Young Choi, Jinseu Park

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.9field-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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  10. Effects ofPharmaceuticals (Basel, Switzerland) · 2018
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  13. JS-III-49, a hydroquinone derivative, exerts anti-inflammatory activity by targeting Akt and p38.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017
    Article
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  18. Tat-DJ-1 inhibits oxidative stress-mediated RINm5F cell death through suppression of NF-κB and MAPK activation.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents
    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

4 authors at 1 institution in 1 country.

Won Yong SeoDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.
Gi Soo YounDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.
Soo Young ChoiDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.
Jinseu ParkDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 24252, Korea.
Hallym University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Up-regulation of cell adhesion molecules and pro-inflammatory cytokines contributes to enhanced monocyte adhesiveness and infiltration into the skin, during the pathogenesis of various inflammatory skin diseases, including atopic dermatitis. In this study, we examined the anti-inflammatory effects of butein, a tetrahydroxychalcone, and its action mechanisms using TNF-α-stimulated keratinocytes. Butein significantly inhibited TNF-α-induced ICAM-I expression and monocyte adhesion in human keratinocyte cell line HaCaT. Butein also decreased TNF-α-induced pro-inflammatory mediators, such as IL-6, IP-10 and MCP-1, in HaCaT cells. Butein decreased TNF-α-induced ROS generation in a dose-dependent manner in HaCaT cells. In addition, treatment of HaCaT cells with butein suppressed TNF-α-induced MAPK activation. Furthermore, butein suppressed TNF-α-induced NF-kappaB activation. Overall, our results indicate that butein has immunomodulatory activities by inhibiting expression of pro-inflammatory mediators in keratinocytes. Therefore, butein may be used as a therapeutic agent for the treatment of inflammatory skin diseases.

Indexed as

Cell AdhesionCell LineChalconesCytokinesHumansInflammation MediatorsIntercellular Adhesion Molecule-1KeratinocytesMitogen-Activated Protein Kinase 1MonocytesNF-kappa BReactive Oxygen SpeciesSignal TransductionTumor Necrosis Factor-alphaUp-RegulationbuteinChalconesCytokinesInflammation MediatorsIntercellular Adhesion Molecule-1Mitogen-Activated Protein Kinase 1NF-kappa BReactive Oxygen SpeciesTumor Necrosis Factor-alpha

Identifiers

PMID25541056
PMCPMC4641232
OpenAlexW2320997035

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.