Evidence map›Paper›PMID 22111069›Full record

ArticleChonnam medical journal2011

Theaflavin Inhibits LPS-Induced IL-6, MCP-1, and ICAM-1 Expression in Bone Marrow-Derived Macrophages Through the Blockade of NF-κB and MAPK Signaling Pathways.

Seewan Kim, Young-Eun Joo

Open access · hybridAbstract read
In one paragraph

Article in Chonnam medical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 55 citations in OpenAlex.

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  19. Tea and bone health: steps forward in translational nutrition.The American journal of clinical nutrition · 2013
    Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Seewan KimKorean Minjok Leadership Academy, Hoengseong, Korea.
Young-Eun Joo
Chonnam National University · KRKorean Nurses Association · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Theaflavin, the main polyphenol in black tea, has anti-inflammatory, antioxidative, anti-mutagenic, and anti-carcinogenic properties. The aim of this study was to evaluate the effects of theaflavin on lipopolysaccharide (LPS)-induced innate signaling and expression of pro-inflammatory mediators in bone marrow-derived macrophages isolated from ICR mice. The effects of theaflavin on the expression of proinflammatory mediators, LPS-induced nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways were examined by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunofluorescence. LPS-induced interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) expression was inhibited by theaflavin. LPS-induced inhibitor kappa B alpha (IκBα) degradation and nuclear translocation of RelA were blocked by theaflavin. LPS-induced phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK), and p38 MAPK was inhibited by theaflavin. The inhibitory effect of theaflavin on IL-6, MCP-1, and ICAM-1 expression was completely inhibited by Bay11-7082 (NF-κB inhibitor). The inhibitory effect of theaflavin on IL-6 and ICAM-1 expression was inhibited by SB203580 (p38 MAPK inhibitor). The inhibitory effect of theaflavin on MCP-1 expression was inhibited by SP600125 (JNK inhibitor). These results indicate that theaflavin prevents LPS-induced IL-6, MCP-1, and ICAM-1 expression through blockade of NF-κB and MAPK signaling pathways in bone marrow-derived macrophages.

Indexed as

MacrophageMAP kinaseNF-kappa BTheaflavin

Identifiers

PMID22111069
PMCPMC3214874
OpenAlexW2150574201

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.