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DOI 10.3390/vetsci13060549

Медицинская библиотека · Veterinary sciences · 2026

Ferulic Acid Prevents the Hepatotoxicity of AFB1 on Broilers via Regulating Autophagy.

Zhang Bo, Jiang Lijia, Zuo Yuanyuan, Zhang Hong, Wang Xinghe, Wu Changde

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Аннотация

Aflatoxin B1 (AFB1), a common contaminant in broiler feed, impairs hepatic function and poses a significant threat to the poultry industry by disrupting cellular autophagy. Ferulic acid (FA) is a naturally occurring phenolic compound with antioxidant, anti-inflammatory, and autophagy-modulating properties. However, whether FA alleviates AFB1-induced autophagy impairment in broiler liver remains unclear. In this study, an AFB1-induced liver injury model was established. A series of experiments were conducted to evaluate the effects of AFB1 and FA on autophagy-related processes. The results showed that AFB1 exposure was associated with reduced expression of autophagy-related markers, including ULK1, ATG14, ATG5, and LC3-II/LC3-I ratio, suggesting alterations in autophagy-related processes associated with autophagosome formation and maturation. FA supplementation partially reversed these changes and alleviated ultrastructural liver damage induced by AFB1. Transcriptomic and western blot analyses further demonstrated that AFB1 exposure increased p53 expression, dysregulated the BRAF/ERK1/ERK2/mTOR signaling pathway, increased p70S6K expression, and decreased 4E-BP1 expression. FA supplementation alleviated these changes. These results showed that FA may alleviate AFB1-induced alterations in autophagy-related biomarkers in broiler liver, accompanied by changes in the BRAF/ERK1/ERK2/mTOR signaling pathway, suppression of p70S6K expression, and restoration of 4E-BP1 expression, which may contribute to its protective effects against AFB1-induced liver toxicity in broilers.

Для цитирования: Zhang Bo, Jiang Lijia, Zuo Yuanyuan, Zhang Hong, Wang Xinghe, Wu Changde. Ferulic Acid Prevents the Hepatotoxicity of AFB1 on Broilers via Regulating Autophagy.. Veterinary sciences. 2026. DOI: 10.3390/vetsci13060549.
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