Evidence map›Paper›PMID 24587411›Full record

ArticlePloS one2014

Luteolin inhibits human keratinocyte activation and decreases NF-κB induction that is increased in psoriatic skin.

Zuyi Weng, Arti B Patel, Magdalini Vasiadi, Anastasia Therianou, Theoharis C Theoharides

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 88 citations in OpenAlex.

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  11. The Promising Role of Polyphenols in Skin Disorders.Molecules (Basel, Switzerland) · 2024
    Review
  12. Article
  13. Luteolin Alleviates the TNF-Mediators of inflammation · 2024
    Article
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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 at 3 institutions in 2 countries.

Zuyi WengMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America ; Graduate Program in Pharmacology and Experimental Therapeutics, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America.
Arti B PatelMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America ; Graduate Program in Biochemistry, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America.
Magdalini VasiadiMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America ; Graduate Program in Pharmacology and Experimental Therapeutics, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America.
Anastasia TherianouFirst Department of Dermatology, A. Sygros Hospital, Athens University Medical School, Athens, Greece.
Theoharis C TheoharidesMolecular Immunopharmacology and Drug Discovery Laboratory, Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America ; Graduate Program in Pharmacology and Experimental Therapeutics, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America ; Graduate Program in Biochemistry, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts, United States of America ; Department of Internal Medicine, Tufts University School of Medicine and Tufts Medical Center, Boston, Massachusetts, United States of America.
Tufts University · USAndreas Sygros Hospital · GRTufts Medical Center · US

Funding

Stress Induces Skin Mast Cell Activation &VasodilationR01AR047652 · NIAMS · TUFTS UNIVERSITY BOSTON · PI THEOHARIDES, THEOHARIS C. · 2001 to 2011
$3.0M
NIAMS NIH HHS AR47652NIAMS NIH HHS R01 AR047652
6 · The paper itself

Abstract

Psoriasis (Ps) is an autoimmune disease characterized by keratinocyte hyperproliferation and chronic inflammation, with increased expression of tumor necrosis factor (TNF) and vascular endothelial growth factor (VEGF). Anti-TNF biologic agents are effective in treating Ps, but are associated with increased risk of infections and blood malignancies. Moreover, keratinocyte hyperproliferation and activation have yet to be addressed. Flavonoids, such as luteolin, are natural compounds with potent anti-inflammatory properties, but their actions on keratinocytes remain unknown. We show that TNF (50 ng/mL) triggers significant production of inflammatory mediators interleukin-6, interleukin-8 and VEGF from both human HaCaT and primary keratinocytes. Pretreatment with the flavonoid luteolin (10-100 µM) significantly inhibits mRNA expression and release of all three mediators in a concentration-dependent manner. More importantly, luteolin decreases TNF-induced phosphorylation, nuclear translocation and DNA binding of the nuclear factor-kappa B (NF-κB) typically involved in inflammatory mediator transcription. We also report that luteolin reduces TNF-induced mRNA expression of two genes (NFKB1 and RELA) encoding two NF-κB subunits (NF-κB p50 and NF-κB p65, respectively). Interestingly, we show that gene expression of RELA is increased in human psoriatic skin. Keratinocyte proliferation, which is a characteristic feature of psoriatic skin, is effectively reduced by luteolin in HaCaT cells, but not in primary keratinocytes. Finally, luteolin does not affect intracellular ATP production or viability. Appropriate formulations of luteolin and related flavones may be promising candidates to be developed into local and systemic treatments for Ps and other inflammatory skin diseases.

Indexed as

Active Transport, Cell NucleusAdenosine TriphosphateAdultBlotting, WesternCell LineCell NucleusCell ProliferationCells, CulturedGene ExpressionHumansInterleukin-6Interleukin-8KeratinocytesLuteolinNF-kappa BPhosphorylationAdenosine TriphosphateInterleukin-6Interleukin-8LuteolinNF-kappa BRELA protein, humanTranscription Factor RelATumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID24587411
PMCPMC3938790
OpenAlexW1976639539

What OpenQuestion holds

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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.