Evidence map›Paper›PMID 26660901›Full record

ArticlePloS one2015

Brazilian Red Propolis Attenuates Inflammatory Signaling Cascade in LPS-Activated Macrophages.

Bruno Bueno-Silva, Dione Kawamoto, Ellen S Ando-Suguimoto, Severino M Alencar, Pedro L Rosalen, Marcia P A Mayer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Review
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  15. Article
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  17. Article
  18. Anti-Inflammatory Effects of (3Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  19. Review
  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

6 authors at 2 institutions in 2 countries.

Bruno Bueno-SilvaDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Dione KawamotoDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Ellen S Ando-SuguimotoDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Severino M AlencarCollege of Agriculture "Luiz de Queiroz" (ESALQ/USP), Piracicaba, SP, Brazil.
Pedro L RosalenPiracicaba Dental School, University of Campinas-UNICAMP, Department of Physiologic Sciences, Piracicaba, SP, Brazil.
Marcia P A MayerDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Universidade de São Paulo · BRMethodist University of Piracicaba · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although previous studies suggested an anti-inflammatory property of Brazilian red propolis (BRP), the mechanisms involved in the anti-inflammatory effects of BRP and its activity on macrophages were still not elucidated. This study aimed to evaluate whether BRP attenuates the inflammatory effect of LPS on macrophages and to investigate its underlying mechanisms. BRP was added to RAW 264.7 murine macrophages after activation with LPS. NO production, cell viability, cytokines profile were evaluated. Activation of inflammatory signaling pathways and macrophage polarization were determined by RT-qPCR and Western blot. BRP at 50 μg/ml inhibited NO production by 78% without affecting cell viability. Cd80 and Cd86 were upregulated whereas mrc1 was down regulated by BRP indicating macrophage polarization at M1. BRP attenuated the production of pro-inflammatory mediators IL-12, GM-CSF, IFN-Ɣ, IL-1β in cell supernatants although levels of TNF- α and IL-6 were slightly increased after BRP treatment. Levels of IL-4, IL-10 and TGF-β were also reduced by BRP. BRP significantly reduced the up-regulation promoted by LPS of transcription of genes in inflammatory signaling (Pdk1, Pak1, Nfkb1, Mtcp1, Gsk3b, Fos and Elk1) and of Il1β and Il1f9 (fold-change rate > 5), which were further confirmed by the inhibition of NF-κB and MAPK signaling pathways. Furthermore, the upstream adaptor MyD88 adaptor-like (Mal), also known as TIRAP, involved in TLR2 and TLR4 signaling, was down- regulated in BRP treated LPS-activated macrophages. Given that BRP inhibited multiple signaling pathways in macrophages involved in the inflammatory process activated by LPS, our data indicated that BRP is a noteworthy food-source for the discovery of new bioactive compounds and a potential candidate to attenuate exhacerbated inflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory AgentsBrazilCell LineCell SurvivalCytokinesDown-RegulationLipopolysaccharidesLymphocyte ActivationMacrophagesMembrane GlycoproteinsMiceMitogen-Activated Protein KinasesNF-kappa BNitric OxidePropolisAnti-Inflammatory AgentsCytokinesLipopolysaccharidesMembrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa BNitric OxidePropolisReceptors, Interleukin-1TIRAP protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID26660901
PMCPMC4684384
OpenAlexW2197775693

What OpenQuestion holds

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Registered trials

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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.