Evidence map›Paper›PMID 40278676›Full record

ArticleToxins2025

Insights from Metabolomic and Transcriptomic Analyses into Sulforaphane's Protective Mechanism Against Deoxynivalenol Toxicity via Spermine Regulation.

Yeyi Xiao, Jianliang Wu, Menke Feng, Jie Wang, Lele Qi, Chao Xu, Haifei Wang, Wenbin Bao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxins, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

8 authors.

Yeyi XiaoKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Jianliang WuBeijing Zhongyu Pig Breeding Co., Ltd., Beijing 100194, China.
Menke FengKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Jie WangKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Lele QiKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Chao XuKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.
Haifei WangKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.ORCID 0000-0003-2424-9743
Wenbin BaoKey Laboratory for Animal Genetics, Breeding, Reproduction and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China.ORCID 0000-0001-5486-2253

Funding

Biological Breeding-National Science and Technology Major Project 2023ZD04044National Natural Science Foundation of China 32372837Postgraduate Research & Practice Innovation Program of Jiangsu Province Yangzhou University: KYCX22_3530
6 · The paper itself

Abstract

Deoxynivalenol (DON) is a mycotoxin ubiquitously present in the environment. Emerging evidence demonstrated that sulforaphane (SFN) exerts potent protective effects against DON-triggered cytotoxicity through multimodal mechanisms. This study aimed to investigate the protective mechanism of SFN during DON exposure. Untargeted metabolomics of IPEC-J2 cells revealed a total of 399 differential metabolites between the DON and control group and 365 differential metabolites between the SFN + DON and DON group. KEGG enrichment was performed to investigate the potential regulatory pathways. The transcriptome identified a total of 1839 differential expression genes (DEGs) between DON and SFN + DON groups. This result indicated that DON exposure and SFN treatment have a profound impact on cellular metabolism and genes. Integrated analysis of the transcriptome and metabolome showed that spermine was a potential biomarker for SFN treatment. SFN increased spermine abundance by regulating genes in glutathione, beta-alanine, and arginine and proline metabolism pathways. Functional experiments demonstrated that spermine alleviated DON-induced oxidative stress, as evidenced by increased cell viability, reduced ROS levels, restored mitochondrial membrane potential (ΔΨm), and normalized antioxidant enzyme activity. Moreover, spermine significantly decreased the cell apoptosis rate induced by DON, which suggested that spermine significantly alleviated the DON-induced cytotoxicity. Overall, these findings elucidated the protective role of SFN through spermine-related mechanisms against the toxicity of DON.

Indexed as

IsothiocyanatesSpermineSulfoxidesTranscriptomeTrichothecenesAnimalsApoptosisCell LineCell SurvivalGene Expression ProfilingMembrane Potential, MitochondrialMetabolomeMetabolomicsOxidative StressdeoxynivalenolIsothiocyanatesSperminesulforaphaneSulfoxidesTrichothecenesdeoxynivalenolmetaboliteoxidative stresssperminesulforaphane

Identifiers

PMID40278676
PMCPMC12031357

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.