Evidence map›Paper›PMID 32787484›Full record

ArticleImmunopharmacology and immunotoxicology2020

Bromosulfophthalein suppresses inflammatory effects in lipopolysaccharide-stimulated RAW264.7 macrophages.

Fuai Cui, Sean B Sequeira, Zhenyue Huang, Guowei Shang, Quanjun Cui, Xinlin Yang

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunopharmacology and immunotoxicology, 2020. 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
0.5field-weighted citation impact, top 37% 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, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Engineering a Pseudo-26-kDaBiomolecules · 2021
    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 1 institution in 2 countries.

Fuai CuiDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
Sean B SequeiraDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
Zhenyue HuangDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
Guowei ShangDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
Quanjun CuiDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
Xinlin YangDepartment of Orthopaedic Surgery, University of Virginia, Charlottesville, VA, USA.
University of Virginia · US

Funding

A novel inflammation targeting Tc-99m probe for osteoarthritis imagingR21AR070987 · NIAMS · UNIVERSITY OF VIRGINIA · PI CUI, QUANJUN, PAN, DONGFENG · 2017 to 2018
$390k
NIAMS NIH HHS R21 AR070987
6 · The paper itself

Abstract

objectiveIt has been reported that glutathione (GSH), the most abundant cellular antioxidant, can inhibit production of pro-inflammatory cytokines by activated macrophages. Bromosulfophthalein (BSP) has been recognized as an inhibitor of the efflux of reduced GSH from cells, leading to an increase in the intracellular GSH level. In this study, we evaluated, for the first time, whether BSP possessed anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated macrophages. MATERIALS AND

methodsRAW 264.7 cells were treated with BSP and the levels of proinflammatory cytokines, GSH, and nitrite were assessed. Gene expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF α), interleukin-1beta (IL-1β), and interleukin-6 (IL-6) was analyzed via quantitative RT-PCR. We also examined various inflammatory signaling pathways including Akt/forkhead box protein O1 (FoxO1)/toll-like receptor 4 (TLR4), mitogen-activated protein kinases (MAPKs), and Fas protein by Western blot and flow cytometry analysis.

resultsOur study demonstrated that BSP induced an increase in intracellular GSH level in LPS-stimulated macrophages. BSP inhibited production of nitric oxide and proinflammatory cytokines. BSP increased phosphorylation of Akt and nuclear exclusion of FoxO1 and suppressed TLR4 expression. Additionally, BSP decreased MAPKs activation and Fas expression. DISCUSSION AND

conclusionTaken together, these data suggest that BSP can attenuate inflammation through multiple signaling pathways. These findings highlight the potential of BSP as a new anti-inflammatory agent.

Indexed as

AnimalsAnti-Inflammatory AgentsCytokinesfas ReceptorForkhead Box Protein O1Inflammation MediatorsLipopolysaccharidesMacrophage ActivationMacrophagesMiceMitogen-Activated Protein KinasesNitric OxideNitric Oxide Synthase Type IIPhosphorylationProto-Oncogene Proteins c-aktRAW 264.7 CellsAnti-Inflammatory AgentsCytokinesFas protein, mousefas ReceptorForkhead Box Protein O1Foxo1 protein, mouseInflammation MediatorsLipopolysaccharidesMitogen-Activated Protein KinasesNitric OxideNitric Oxide Synthase Type IINos2 protein, mouseProto-Oncogene Proteins c-aktSulfobromophthaleinTlr4 protein, mouseToll-Like Receptor 4Bromosulfophthaleinglutathioneinflammatory responsesmacrophagessignal pathways

Identifiers

PMID32787484
PMCPMC7773219
OpenAlexW3048769522

What OpenQuestion holds

Textmetadata
LicenceTDM
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.