The Protective Effects of Lycopene Against T2 Mycotoxin-Induced Apoptosis in Mouse Liver and Its Transcriptional Mechanisms
7 affiliations
- 1Jiangsu Key Laboratory of Animal Genetic Breeding and Molecular Design, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
- 2College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China
- 3Jiangsu Interdisciplinary Center for Zoonoses and Biosafety, Yangzhou University, Yangzhou 225009, China
- 4Faculty of Science and Agriculture, University of Limpopo, Sovenga 0727, South Africa
- 5Department of Animal Resource and Science, Dankook University, Cheonan 31116, Republic of Korea
- 6Department of Veterinary Biomedical Sciences, Botswana University of Agriculture and Natural Resources, Gaborone 0027, Botswana
- 7Guangling College, Yangzhou University, Yangzhou 225009, China
Abstract
Background: T-2 toxin, a highly toxic Fusarium-derived mycotoxin, frequently contaminates feed and poses significant risks to livestock production and food safety by inducing severe apoptotic damage in the liver, which is the primary organ responsible for toxin metabolism and detoxification. Lycopene, a natural carotenoid antioxidant, exhibits possible hepatoprotective effects against various exogenous toxins; however, there are currently few studies that analyze, from a transcriptomic perspective, how lycopene mitigates T-2 toxin-induced apoptosis in liver tissue. Methods: mouse model of T-2 toxin exposure was established, with low- and high-dose lycopene co-administered for 5 weeks. Results: Transcriptomic analysis and TUNEL staining demonstrated that T-2 toxin stimulation induced marked activation of apoptotic-signaling pathways in liver tissue, while lycopene intervention significantly suppressed this transcriptional activation and alleviated T-2 toxin-provoked hepatocyte DNA-fragmentation signals, together with decreased transcription of pro-apoptotic genes. Comprehensive investigation revealed that T-2 toxin upregulated the RORC (RAR related orphan receptor C) and enhanced its occupancy at the promoter regions of apoptosis-related genes (TNFSF10, PMAIP1, IL18, and RNASEL), as verified by ChIP-qPCR assays. Lycopene strongly reversed the T-2 toxin-induced increase in RORC expression and its binding to apoptosis-related gene promoters. Analysis of the protein—protein interaction network further revealed potential molecular links between RORC and multiple core apoptotic pathway components. Conclusions: Lycopene protects mouse liver from T-2 toxin-induced apoptotic injury, while RORC is identified as a potential candidate regulatory factor associated with this protective effect. This study provides experimental evidence at the transcriptomic level for the use of lycopene in the prevention and treatment of liver tissue damage caused by T-2 toxin.
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BibTeX
@article{zhu2026protective,
title = {{The Protective Effects of Lycopene Against T2 Mycotoxin-Induced Apoptosis in Mouse Liver and Its Transcriptional Mechanisms}},
author = {Chuyang Zhu and Long Yuan and Cuipeng Zhu and Yunhan Wang and Xiaoyue Yuan and Yujuan Cai and Shifeng Pan and Tlou Grace Manyelo and Thobela Louis Tyasi and In Ho Kim and Abdelkareem A. Ahmed and Hao-Yu Liu and Demin Cai},
journal = {Metabolites},
year = {2026},
month = oct,
doi = {10.3390/metabo16110815},
url = {https://www.mdpi.com/2218-1989/16/11/815},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Protective Effects of Lycopene Against T2 Mycotoxin-Induced Apoptosis in Mouse Liver and Its Transcriptional Mechanisms
AU - Chuyang Zhu
AU - Long Yuan
AU - Cuipeng Zhu
AU - Yunhan Wang
AU - Xiaoyue Yuan
AU - Yujuan Cai
AU - Shifeng Pan
AU - Tlou Grace Manyelo
AU - Thobela Louis Tyasi
AU - In Ho Kim
AU - Abdelkareem A. Ahmed
AU - Hao-Yu Liu
AU - Demin Cai
PY - 2026
DA - 2026/10/27
JO - Metabolites
DO - 10.3390/metabo16110815
UR - https://www.mdpi.com/2218-1989/16/11/815
AB - Background: T-2 toxin, a highly toxic Fusarium-derived mycotoxin, frequently contaminates feed and poses significant risks to livestock production and food safety by inducing severe apoptotic damage in the liver, which is the primary organ responsible for toxin metabolism and detoxification. Lycopene, a natural carotenoid antioxidant, exhibits possible hepatoprotective effects against various exogenous toxins; however, there are currently few studies that analyze, from a transcriptomic perspective, how lycopene mitigates T-2 toxin-induced apoptosis in liver tissue. Methods: mouse model of T-2 toxin exposure was established, with low- and high-dose lycopene co-administered for 5 weeks. Results: Transcriptomic analysis and TUNEL staining demonstrated that T-2 toxin stimulation induced marked activation of apoptotic-signaling pathways in liver tissue, while lycopene intervention significantly suppressed this transcriptional activation and alleviated T-2 toxin-provoked hepatocyte DNA-fragmentation signals, together with decreased transcription of pro-apoptotic genes. Comprehensive investigation revealed that T-2 toxin upregulated the RORC (RAR related orphan receptor C) and enhanced its occupancy at the promoter regions of apoptosis-related genes (TNFSF10, PMAIP1, IL18, and RNASEL), as verified by ChIP-qPCR assays. Lycopene strongly reversed the T-2 toxin-induced increase in RORC expression and its binding to apoptosis-related gene promoters. Analysis of the protein—protein interaction network further revealed potential molecular links between RORC and multiple core apoptotic pathway components. Conclusions: Lycopene protects mouse liver from T-2 toxin-induced apoptotic injury, while RORC is identified as a potential candidate regulatory factor associated with this protective effect. This study provides experimental evidence at the transcriptomic level for the use of lycopene in the prevention and treatment of liver tissue damage caused by T-2 toxin.
SN - 2218-1989
ER -