Evidence map›Paper›PMID 39269625›Full record

ArticlePlant foods for human nutrition (Dordrecht, Netherlands)2024

Nomilin Reversed Cardiotoxicity Caused by Co-exposure to Zearalenone and Deoxynivalenol via the Keap1/Nrf2 Signaling Pathway in Zebrafish.

Xing Liu, Yuting Peng, Ruobing Chen, Yueyue Zhou, Mingzhu Xia, Xinyi Wu, Meng Yu

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Article in Plant foods for human nutrition (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xing Liu *School of Public Health, Yangzhou University, Yangzhou, 225009, China. liuxing@yzu.edu.cn.
Yuting Peng *School of Public Health, Yangzhou University, Yangzhou, 225009, China.
Ruobing ChenSchool of Public Health, Yangzhou University, Yangzhou, 225009, China.
Yueyue ZhouSchool of Public Health, Yangzhou University, Yangzhou, 225009, China.
Mingzhu XiaSchool of Public Health, Yangzhou University, Yangzhou, 225009, China.
Xinyi WuSchool of Public Health, Yangzhou University, Yangzhou, 225009, China.
Meng YuDepartment of Otorhinolaryngology-Head and Neck Surgery, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, 225009, China. mengyu0716@yeah.net.

Funding

National Natural Science Foundation of China 81903357
6 · The paper itself

Abstract

The contamination of food and feed by mycotoxins, particularly zearalenone (ZEA) and deoxynivalenol (DON), is a global issue. Prenatal exposure to ZEA and DON can result in congenital cardiac malformations in fetuses. Addressing the prevention and mitigation of embryonic cardiotoxicity caused by these toxins is crucial. Citrus limonoid nomilin (NOM) is an extract known for its pathological properties in various diseases. This study investigated the potential mechanism of NOM in mitigating cardiotoxicity caused by ZEA and DON co-exposure in a zebrafish model. The findings indicated that NOM pretreatment alleviated cardiac developmental toxicity induced by ZEA and DON and normalized the expression of key genes involved in heart development, including gata4, vmhc, nkx2.5, and sox9b. Co-exposure to NOM, ZEA, and DON enhanced SOD and catalase activity, increased glutathione levels, and reduced ROS and malondialdehyde production. Furthermore, NOM reduced cardiac oxidative damage by activating the Keap1/Nrf2 signaling pathway. In summary, this study offers new insights for preventive interventions against congenital heart disease caused by mycotoxin exposure.

Indexed as

CardiotoxicityKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Signal TransductionTrichothecenesZearalenoneZebrafishZebrafish ProteinsAnimalsCarrier ProteinsHeartOxidative StressPlant ExtractsReactive Oxygen SpeciesCarrier ProteinsdeoxynivalenolKeap1a protein, zebrafishKelch-Like ECH-Associated Protein 1nfe2l2a protein, zebrafishNF-E2-Related Factor 2Plant ExtractsReactive Oxygen SpeciesTrichothecenesZearalenoneZebrafish ProteinsCardiotoxicityDeoxynivalenolNomilinNrf2Zearalenone

Identifiers

PMID39269625

What OpenQuestion holds

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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.