Evidence map›Paper›PMID 24340073›Full record

ArticlePloS one2013

Beauvericin ameliorates experimental colitis by inhibiting activated T cells via downregulation of the PI3K/Akt signaling pathway.

Xue-Feng Wu, Rui Xu, Zi-Jun Ouyang, Cheng Qian, Yan Shen, Xu-Dong Wu, Yan-Hong Gu, Qiang Xu, Yang Sun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. A putative ABC transporter gene,Microbiology spectrum · 2025
    Article
  3. The mycotoxin Beauvericin is an uncompetitive inhibitor of Cathepsin B.Protein science : a publication of the Protein Society · 2025
    Article
  4. Review
  5. Journal of natural products · 2024
    Article
  6. Article
  7. Review
  8. Genotoxicity of beauvericin.EFSA journal. European Food Safety Authority · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Renshen Baidu powder protects ulcerative colitisFrontiers in pharmacology · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Secondary metabolites (SMs) ofRSC advances · 2018
    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

9 authors at 2 institutions in 1 country.

Xue-Feng WuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu Province, China.
Rui Xu
Zi-Jun Ouyang
Cheng Qian
Yan Shen
Xu-Dong Wu
Yan-Hong Gu
Qiang Xu
Yang Sun
Nanjing University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crohn's disease is a common, chronic inflammatory bowel condition characterized by remission and relapse. Accumulating evidence indicates that activated T cells play an important role in this disease. In the present study, we aimed to examine the effect of beauvericin, a natural cyclic peptide, on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice, which mimics Crohn's disease. Beauvericin significantly reduced weight loss, diarrhea and mortality, accompanied with notable alleviation of macroscopic and microscopic signs. In addition, this compound decreased serum levels of tumor necrosis factor (TNF)-α and interferon (IFN)-γ in a concentration-dependent manner in mice with experimental colitis. These effects of beauvericin are attributed to its inhibition on activated T cells. Flow cytometry and immunoblot assay data showed that beauvericin suppressed T-cell proliferation, activation and IFN-γ-STAT1-T-bet signaling and subsequently led to apoptosis of activated T cells by suppressing Bcl-2 and phosphorylated Bad as well as increasing cleavage of caspase-3, -9, -12 and PARP. Furthermore, inhibition of PI3K/Akt signaling, which was an upstream regulator of cell activation and survival in activated T cells, contributed to the effect of beauvericin. Overall, these results supported beauvericin as a novel drug candidate for the treatment of colonic inflammation mainly by targeting PI3K/Akt in activated T cells.

Indexed as

Gene Expression Regulation, EnzymologicSignal TransductionAnimalsApoptosisCell ProliferationColitisDepsipeptidesDisease Models, AnimalDown-RegulationFemaleFlow CytometryInflammationInterferon-gammaLymphocyte ActivationMembrane Potential, MitochondrialMicebeauvericinDepsipeptidesInterferon-gammaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alpha

Identifiers

PMID24340073
PMCPMC3858350
OpenAlexW2093066464

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.