Fish Oil Ameliorates Deoxynivalenol-Induced Liver Injury Through Modulating Ferroptosis Signaling Pathway in Weaned Pigs

content, and increased hepatic glutathione (GSH) content. Moreover, dietary FO ameliorated ultrastructural liver damage induced by DON. Furthermore, DON significantly downregulated the mRNA levels of multiple genes associated with iron metabolism and ferroptosis, including heat shock protein beta-1 (HSPB1), acyl-CoA synthetase long chain family member 4 (ACSL4), and arachidonate 15-lipoxygenase (ALOX15), and upregulated the mRNA levels of transferrin (TF), ferritin heavy chain (FTH), solute carrier family 7 member 11 (SLC7A11), and transferrin receptor 1 (TFR1). Dietary FO counteracted these alterations by decreasing the mRNA of SLC7A11, TFR1, FTH, and TF after DON exposure. Finally, FO significantly decreased the protein expression of SLC7A11, iron-responsive element-binding protein 2 (IREB2), and FHT1 and increased the GPX4 protein expression following DON exposure. These findings suggest that FO may ameliorate DON-induced liver injury in weaned piglets, possibly through suppressing the ferroptosis signaling pathway.

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Publication Details

Journal
Animals
Published
2026-04-17
DOI
https://doi.org/10.3390/ani16081234
Primary Topic
Ferroptosis and cancer prognosis
Type
article
Field-Weighted Citation Impact
0.00

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article

Fish Oil Ameliorates Deoxynivalenol-Induced Liver Injury Through Modulating Ferroptosis Signaling Pathway in Weaned Pigs

Mohan Zhou, Jiasi Liu, Shaokui Chen, Junjie Guo et al.
Animals
Ferroptosis and cancer prognosis
article

Fish Oil Ameliorates Deoxynivalenol-Induced Liver Injury Through Modulating Ferroptosis Signaling Pathway in Weaned Pigs

Mohan Zhou, Jiasi Liu, Shaokui Chen, Junjie Guo, Minfang Zhang, Kan Xiao, Yulan Liu
article en

Abstract

content, and increased hepatic glutathione (GSH) content. Moreover, dietary FO ameliorated ultrastructural liver damage induced by DON. Furthermore, DON significantly downregulated the mRNA levels of multiple genes associated with iron metabolism and ferroptosis, including heat shock protein beta-1 (HSPB1), acyl-CoA synthetase long chain family member 4 (ACSL4), and arachidonate 15-lipoxygenase (ALOX15), and upregulated the mRNA levels of transferrin (TF), ferritin heavy chain (FTH), solute carrier family 7 member 11 (SLC7A11), and transferrin receptor 1 (TFR1). Dietary FO counteracted these alterations by decreasing the mRNA of SLC7A11, TFR1, FTH, and TF after DON exposure. Finally, FO significantly decreased the protein expression of SLC7A11, iron-responsive element-binding protein 2 (IREB2), and FHT1 and increased the GPX4 protein expression following DON exposure. These findings suggest that FO may ameliorate DON-induced liver injury in weaned piglets, possibly through suppressing the ferroptosis signaling pathway.

AnimalsVol. 16(8)
Wuhan Polytechnic University (CN)
National Natural Science Foundation of China, Natural Science Foundation of Hubei Province, Wuhan Polytechnic University
Openalex Percentile: Top 21%
Ferroptosis and cancer prognosis
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