Evidence map›Paper›PMID 22862554›Full record

ArticleImmunology2012

5,7-Dihydroxy-3,4,6-trimethoxyflavone inhibits intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 via the Akt and nuclear factor-κB-dependent pathway, leading to suppression of adhesion of monocytes and eosinophils to bronchial epithelial cells.

Jireh Jung, Su H Ko, Do Y Yoo, Jin Y Lee, Yeong-Jeon Kim, Seul M Choi, Kyung K Kang, Ho J Yoon, Hyeyoung Kim, Jeehee Youn and 1 more

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Eupatilin downregulates phorbol 12-myristate 13-acetate-inducedThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
    Article
  12. Article
  13. Colorectal cancer: The epigenetic role of microbiome.World journal of clinical cases · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 4 institutions in 1 country.

Jireh JungDepartments of Microbiology and Biomedical Science, Hanyang University College of Medicine and Hanyang University Graduate School of Biomedical Science and Engineering, Seoul, South Korea.
Su H Ko
Do Y Yoo
Jin Y Lee
Yeong-Jeon Kim
Seul M Choi
Kyung K Kang
Ho J Yoon
Hyeyoung Kim
Jeehee Youn
Jung M Kim
Hanyang University · KRDong-A Pharmaceutical (South Korea) · KRJoongbu University · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

5,7-Dihydroxy-3',4',6'-trimethoxyflavone (eupatilin), the active pharmacological ingredient from Artemisia asiatica Nakai (Asteraceae), is reported to have a variety of anti-inflammatory properties in intestinal epithelial cells. However, little information is known about the molecular mechanism of eupatilin-induced attenuation of bronchial epithelial inflammation. This study investigates the role of eupatilin in the adhesion of inflammatory cells such as monocytes and eosinophils to bronchial epithelial cells. Stimulation of a human bronchial epithelial cell line (BEAS-2B) with tumour necrosis factor-α (TNF-α) increased the expression of surface adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), in which eupatilin significantly inhibited the expression of those adhesion molecules in a dose-dependent manner. Eupatilin suppressed the TNF-α-induced activation of IκBα and nuclear factor-κB (NF-κB) signals in BEAS-2B cells. The IκB kinase (IKK) activation was also significantly reduced in eupatilin-pre-treated BEAS-2B and primary normal human bronchial epithelial (NHBE) cells. However, eupatilin did not influence AP-1 activity in TNF-α-stimulated cells. Suppression of NF-κB signalling induced by eupatilin resulted in the inhibition of the expression of adhesion molecules and the adhesion of monocytes and eosinophils to BEAS-2B cells. Furthermore, eupatilin suppressed the phosphorylation of Akt in TNF-α-stimulated BEAS-2B and NHBE cells, leading to down-regulation of NF-κB activation and adhesion molecule expression and finally to suppression of the inflammatory cell adhesion to epithelial cells. These results suggest that eupatilin can inhibit the adhesion of inflammatory cells to bronchial epithelial cells via a signalling pathway, including activation of Akt and NF-κB, as well as expression of adhesion molecules.

Indexed as

AsthmaBronchiCell AdhesionCell LineEosinophilsEpithelial CellsFlavonoidsHumansI-kappa B KinaseI-kappa B ProteinsIntercellular Adhesion Molecule-1MonocytesNF-kappa BNF-KappaB Inhibitor alphaProto-Oncogene Proteins c-aktRespiratory MucosaeupatilinFlavonoidsI-kappa B KinaseI-kappa B ProteinsIntercellular Adhesion Molecule-1NF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanProto-Oncogene Proteins c-aktTranscription Factor AP-1Tumor Necrosis Factor-alphaVascular Cell Adhesion Molecule-1

Identifiers

PMID22862554
PMCPMC3449251
OpenAlexW1968316822

What OpenQuestion holds

Textmetadata
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.