Evidence map›Paper›PMID 35566232›Full record

ArticleMolecules (Basel, Switzerland)2022

5,2'-Dibromo-2,4',5'-trihydroxydiphenylmethanone Inhibits LPS-Induced Vascular Inflammation by Targeting the Cav1 Protein.

Hongxia Yuan, Qianyi Hou, Xiue Feng, Yuanlin Zhang, Fan Yang, Rui Ge, Qingshan Li

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

7 authors at 2 institutions in 1 country.

Hongxia YuanShanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Qianyi HouShanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Xiue FengSchool of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, China.
Yuanlin ZhangShanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Fan YangSchool of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, China.
Rui GeSchool of Pharmaceutical Science, Shanxi Medical University, Taiyuan 030001, China.
Qingshan LiShanxi Key Laboratory of Innovative Drug for the Treatment of Serious Diseases Basing on the Chronic Inflammation, Shanxi University of Chinese Medicine, Jinzhong 030619, China.
Shanxi Medical University · CNShanxi University · CN

Funding

National Natural Science Foundation of China 81473100National Natural Science Foundation of China 82003881National Natural Science Foundation of Shanxi Province 201801D121231National Science and Technology Major Project of China 2018ZX09711001-001-017Science and technology innovation project of universities in Shanxi Province 2019L0718
6 · The paper itself

Abstract

Vascular inflammation is directly responsible for atherosclerosis. 5,2'-Dibromo-2,4',5'-trihydroxydiphenylmethanone (TDD), a synthetic bromophenol derivative, exhibits anti-atherosclerosis and anti-inflammatory effects. However, the underlying pathways are not yet clear. In this study, we first examined the effects of TDD on toll-like receptor-4 (TLR4) activity, the signaling receptor for lipopolysaccharide (LPS), and found that TDD does not inhibit LPS-induced TLR4 expression in EA.hy926 cells and the vascular wall in vivo. Next, we investigated the global protein alterations and the mechanisms underlying the action of TDD in LPS-treated EA.hy926 cells using an isobaric tag for the relative and absolute quantification technique. Western blot analysis revealed that TDD inhibited NF-κB activation by regulating the phosphorylation and subsequent degradation IκBα. Among the differentially expressed proteins, TDD concentration-dependently inhibited Caveolin 1(Cav1) expression. The interaction between Cav1 and TDD was determined by using biolayer interference assay, UV-

Indexed as

AtherosclerosisLipopolysaccharidesAnti-Inflammatory AgentsCaveolin 1HumansInflammationMolecular Docking SimulationNF-kappa BToll-Like Receptor 4Anti-Inflammatory AgentsCaveolin 1LipopolysaccharidesNF-kappa BToll-Like Receptor 45,2′-dibromo-2,4′,5′-trihydroxydiphenylmethanonecaveolin-1EA.hy926 cellslipopolysaccharideNF-κB signalingvascular inflammation

Identifiers

PMID35566232
PMCPMC9101869
OpenAlexW4280509745

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.