Evidence map›Paper›PMID 25059279›Full record

ArticleBMB reports2015

Celastrol ameliorates cytokine toxicity and pro-inflammatory immune responses by suppressing NF-κB activation in RINm5F beta cells.

Sung Mi Ju, Gi Soo Youn, Yoon Shin Cho, Soo Young Choi, Jinseu Park

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
17.8field-weighted citation impact, top 1% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Immunomodulatory properties of triterpenes.Phytochemistry reviews : proceedings of the Phytochemical Society of Europe · 2022
    Review
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  7. Frontiers in pharmacology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Neuroprotective Effect of 3-(Naphthalen-2-Yl(Propoxy)Methyl)Azetidine Hydrochloride on Brain Ischaemia/Reperfusion Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Sung Mi JuDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 200-702, Korea.
Gi Soo YounDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 200-702, Korea.
Yoon Shin ChoDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 200-702, Korea.
Soo Young ChoiDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 200-702, Korea.
Jinseu ParkDepartment of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chunchon 200-702, Korea.
Hallym University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulation of pro-inflammatory mediators contributes to β-cell destruction and enhanced infiltration of immune cells into pancreatic islets during development of type 1 diabetes mellitus. In this study, we examined the regulatory effects and the mechanisms of action of celastrol against cytotoxicity and pro-inflammatory immune responses in the RINm5F rat pancreatic β-cell line stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha, and interferon-γ. Celastrol significantly restored cytokine-induced cell death and significantly inhibited cytokine-induced nitric oxide production. In addition, the protective effect of celastrol was correlated with a reduction in pro-inflammatory mediators, such as inducible nitric oxide synthase, cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly suppressed cytokine- induced signaling cascades leading to nuclear factor kappa B (NF-κB) activation, including IκB-kinase (IKK) activation, IκB degradation, p65 phosphorylation, and p65 DNA binding activity. These results suggest that celastrol may exert its cytoprotective activity by suppressing cytokine-induced expression of pro-inflammatory mediators by inhibiting activation of NF-κB in RINm5F cells.

Indexed as

AnimalsCell LineChemokine CCL2Cyclooxygenase 2CytokinesInflammation MediatorsNF-kappa BNitric OxideNitric Oxide Synthase Type IIPentacyclic TriterpenesRatsTriterpenesCcl2 protein, ratcelastrolChemokine CCL2Cyclooxygenase 2CytokinesInflammation MediatorsNF-kappa BNitric OxideNitric Oxide Synthase Type IIPentacyclic TriterpenesTriterpenes

Identifiers

PMID25059279
PMCPMC4453024
OpenAlexW1993681053

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.