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Article

Curcumin Can Inhibit Zearalenone-Induced Ferroptosis in Porcine Intestinal Epithelial Cells via the p53/SLC7A11/GPX4 Pathway

Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Toxics 2025, 13(9), 713; https://doi.org/10.3390/toxics13090713
Submission received: 21 July 2025 / Revised: 15 August 2025 / Accepted: 23 August 2025 / Published: 24 August 2025

Abstract

Zearalenone (ZEA) is a widely distributed estrogenic mycotoxin that can disrupt intestinal barrier integrity by inducing ferroptosis, thereby posing serious risks to animal health. Curcumin (CUR), as a natural polyphenolic compound with multi-target regulatory properties, has attracted increasing attention for its antioxidative and cytoprotective effects; however, its role in ZEA-induced ferroptosis remains poorly understood. In this study, the protective effects of curcumin (CUR) were evaluated in IPEC-J2 cells by co-treating the cells with zearalenone (ZEA) at its LC50 (75.23 μM) and curcumin (5 or 15 μM) for 24 h. CCK-8 assays showed that CUR significantly (p < 0.05) and highly significantly (p < 0.01) improved cell viability in the 5 μM and 15 μM groups, respectively, compared with ZEA alone. CUR co-treatment significantly (p < 0.01) restored glutathione (GSH) levels, and markedly (p < 0.01) reduced Fe2+ accumulation, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and lipid peroxidation (LPO). Transmission electron microscopy revealed pronounced mitochondrial cristae loss and membrane collapse in ZEA-treated cells, which were visibly alleviated by CUR. At the molecular level, ZEA downregulated GPX4 and SLC7A11 and upregulated ACSL4, FTH1, and p53 (all p < 0.01), whereas these changes were significantly reversed (p < 0.05 or p < 0.01) by CUR. In conclusion, CUR exerts cytoprotective effects against ZEA-induced ferroptosis, likely via modulation of the p53/SLC7A11/GPX4 signaling pathway.
Keywords: zearalenone; curcumin; ferroptosis; lipid peroxidation; IPEC-J2 cells zearalenone; curcumin; ferroptosis; lipid peroxidation; IPEC-J2 cells

Share and Cite

MDPI and ACS Style

Xiong, D.; Qi, W.; Long, M. Curcumin Can Inhibit Zearalenone-Induced Ferroptosis in Porcine Intestinal Epithelial Cells via the p53/SLC7A11/GPX4 Pathway. Toxics 2025, 13, 713. https://doi.org/10.3390/toxics13090713

AMA Style

Xiong D, Qi W, Long M. Curcumin Can Inhibit Zearalenone-Induced Ferroptosis in Porcine Intestinal Epithelial Cells via the p53/SLC7A11/GPX4 Pathway. Toxics. 2025; 13(9):713. https://doi.org/10.3390/toxics13090713

Chicago/Turabian Style

Xiong, Dongwei, Weidong Qi, and Miao Long. 2025. "Curcumin Can Inhibit Zearalenone-Induced Ferroptosis in Porcine Intestinal Epithelial Cells via the p53/SLC7A11/GPX4 Pathway" Toxics 13, no. 9: 713. https://doi.org/10.3390/toxics13090713

APA Style

Xiong, D., Qi, W., & Long, M. (2025). Curcumin Can Inhibit Zearalenone-Induced Ferroptosis in Porcine Intestinal Epithelial Cells via the p53/SLC7A11/GPX4 Pathway. Toxics, 13(9), 713. https://doi.org/10.3390/toxics13090713

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