Evidence map›Paper›PMID 23941302›Full record

ArticleBritish journal of pharmacology2013

Penta-O-galloyl-β-D-glucose ameliorates inflammation by inhibiting MyD88/NF-κB and MyD88/MAPK signalling pathways.

Se-Eun Jang, Supriya R Hyam, Jin-Ju Jeong, Myung Joo Han, Dong-Hyun Kim

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2013. 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
1.5field-weighted citation impact, top 19% 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, 63 citations in OpenAlex.

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  16. Journal of microbiology and biotechnology · 2020
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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 1 institution in 1 country.

Se-Eun JangDepartment of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul, Korea; Department of Food and Nutrition, Kyung Hee University, Seoul, Korea.
Supriya R Hyam
Jin-Ju Jeong
Myung Joo Han
Dong-Hyun Kim
Kyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe gallnut of Rhus chinensis MILL and its main constituent penta-O-galloyl-β-D-glucose (PGG) inhibited NF-κB activation in LPS-stimulated peritoneal and colonic macrophages. Here we have investigated PGG mechanisms underlying anti-inflammatory effects of PGG in vitro and in vivo. EXPERIMENTAL APPROACH: Male C57BL/6 mice (18-22 g, 6 weeks old) were used to prepare peritoneal and colonic macrophages and for the induction of colitis by intrarectal administration of 2,3,4-trinitrobenzene sulphonic acid (TNBS). A range of inflammatory markers and transcription factors were evaluated by elisa, immunoblotting, flow cytometry and confocal microscopy. KEY

resultsExpression of Toll-like receptor (TLR)-4 or Lipopolysaccharide (LPS) binding to TLR-4 in LPS-stimulated peritoneal macrophages was not affected by PGG. However PGG inhibited binding of an anti-MyD88 antibody to peritoneal macrophages, but did not reduce binding of anti-IL-1 receptor-associated kinase (IRAK1) and IRAK4 antibodies to the macrophages with or without transfection with MyD88 siRNA. PGG potently reduced the activation of IRAK1, NF-κB, and MAPKs in LPS- or pepetidoglycan-stimulated peritoneal and colonic macrophages. PGG suppressed IL-1β, TNF-α and IL-6 in LPS-stimulated peritoneal macrophages, while increasing expression of the anti-inflammatorycytokine IL-10. Oral administration of PGG inhibited colon shortening and myeloperoxidase activity in mice with TNBS-induced colitis, along with reducing NF-κB activation and IL-1β, TNF-α, and IL-6 levels, whereas it increased IL-10. CONCLUSIONS AND IMPLICATIONS: PGG reduced activation of NF-κB and MAPK signalling pathways by directly interacting with the MyD88 adaptor protein. PGG may ameliorate inflammatory diseases such as colitis.

Indexed as

Administration, OralAnimalsAnti-Inflammatory AgentsCells, CulturedColitisColonDisease Models, AnimalDose-Response Relationship, DrugGastrointestinal AgentsHydrolyzable TanninsInflammation MediatorsInterleukin-1 Receptor-Associated KinasesMacrophages, PeritonealMaleMAP Kinase Signaling SystemMiceAnti-Inflammatory AgentsGastrointestinal AgentsHydrolyzable TanninsInflammation MediatorsInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseMitogen-Activated Protein KinasesMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BpentagalloylglucoseTlr4 protein, mouseToll-Like Receptor 4Trinitrobenzenesulfonic AcidinflammationmacrophageMyD88NF-κBpenta-O-galloyl-β-D-glucose

Identifiers

PMID23941302
PMCPMC3949655
OpenAlexW1574780512

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.