Evidence map›Paper›PMID 25504111›Full record

ArticleEuropean journal of nutrition2015

Cinnamaldehyde is the main mediator of cinnamon extract in mast cell inhibition.

Yvonne Hagenlocher, Kristina Kiessling, Michael Schäffer, Stephan C Bischoff, Axel Lorentz

Abstract read
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In one paragraph

Article in European journal of nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 35% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Spices and Biomarkers of COVID-19: A Mechanistic and Therapeutic Perspective.Advances in experimental medicine and biology · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Pharmacological treatment options for mast cell activation disease.Naunyn-Schmiedeberg's archives of pharmacology · 2016
    Review
  15. 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

5 authors at 2 institutions in 1 country.

Yvonne HagenlocherDepartment of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany.
Kristina KiesslingDepartment of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany.
Michael SchäfferDepartment of General, Visceral, and Thorax Surgery, Marienhospital Stuttgart, Böheimstraße 37, 70199, Stuttgart, Germany.
Stephan C BischoffDepartment of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany.
Axel LorentzDepartment of Nutritional Medicine, University of Hohenheim, Fruwirthstraße 12, 70593, Stuttgart, Germany. Lorentz@uni-hohenheim.de.
University of Hohenheim · DEMarienhospital Stuttgart · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIn terms of their involvement in allergic and inflammatory conditions, mast cells (MC) can be promising targets for medical agents in therapy. Because of their good compliance and effectiveness, phytochemicals are of great interest as new therapeutic tools in form of nutraceuticals. We found recently that cinnamon extract (CE) inhibits mast cell activation. Here, we analysed the effects of a major compound of CE, cinnamaldehyde (CA), on mast cell activation.

methodsRelease of prestored and de novo synthesised mediators as well as expression of pro-inflammatory cytokines and mast cell-specific proteases were analysed in RBL-2H3 cells or in human mast cells isolated from intestinal tissue (hiMC) treated with CA prior to stimulation by FcεRI crosslinking or IONO/PMA. The results were compared with the corresponding effects of CE.

resultsFollowing treatment with CA, release of β-hexosaminidase in IgE-dependent or IgE-independent activated RBL-2H3 cells was down-regulated in a dose-dependent manner to about 10%. In hiMC, release of β-hexosaminidase was also significantly reduced, and release of LTC4 and CXCL8 was almost completely inhibited by CA. Moreover, IgE-mediated expression of CXCL8, CCL2, CCL3 and CCL4 in hiMC was significantly down-regulated by CA. With the exception of the expression of the mast cell proteases tryptase and chymase, the inhibitory effects of CA were very similar to the effects shown for CE treatment. The reducing effect of CA on mast cell mediators-seen for long- and for short-term incubations-could be related to particular signalling pathways as CA caused a down-regulation in ERK as well as PLCγ1 phosphorylation.

conclusionsCA decreases release and expression of pro-inflammatory mast cell mediators. This inhibitory action is similar to the effects observed for CE indicating CA as the main active compound in CE leading to its anti-allergic properties.

Indexed as

AcroleinAnti-Allergic AgentsAnti-Inflammatory AgentsApoptosisbeta-N-AcetylhexosaminidasesCell LineChemokine CCL2Chemokine CCL3Chemokine CCL4Cinnamomum zeylanicumDown-RegulationHumansImmunoglobulin EInterleukin-8IntestinesLeukotriene C4AcroleinAnti-Allergic AgentsAnti-Inflammatory Agentsbeta-N-AcetylhexosaminidasesCCL2 protein, humanCCL3 protein, humanCCL4 protein, humanChemokine CCL2Chemokine CCL3Chemokine CCL4cinnamaldehydeCXCL8 protein, humanImmunoglobulin EInterleukin-8Leukotriene C4Plant ExtractsReceptors, IgERNA, MessengerAllergyCinnamaldehydeCinnamon extractMast cellsNutraceuticals

Identifiers

PMID25504111
OpenAlexW2030846061

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.