SIRT1 RegulatesFumonisin B1-Induced LMH Cell PANoptosisand Antagonism of Lycopene

Mycotoxin contamination is a universal agricultural problem and a critical health issue. Fumonisin B1 (FB1) is one of the most toxic and extensive fumonisins that exist in various agro-products and foods. Lycopene (LYC), as a natural carotenoid, is becoming increasingly favored owing to its oxidation resistance. Here, we aim to explore the mechanism of FB1-induced hepatotoxicity and the antagonism of LYC. In this study, our findings indicated that FB1 induced mitochondrial structure damage and loss of mitochondrial function in chicken hepatocytes. Furthermore, FB1 upregulated the expression of PANoptosis-related signal molecules. FB1 also reduced the levels of SIRT1 and Ac-FOXO1 protein expression, which then inhibited mitophagy. However, LYC relieved these FB1-induced alterations. Most importantly, SIRT1 knockdown inhibited the protective effects of LYC in FB1-induced mitochondrial damage and PANoptosis. Our study provides evidence for the role of LYC in mycotoxin-induced chicken hepatocyte injury and points to SIRT1 as a potential target for liver protection.

Publication Details

Journal
Figshare
Published
2025-02-12
DOI
https://doi.org/10.1021/acs.jafc.4c11658.s001
Primary Topic
Mycorrhizal Fungi and Plant Interactions
Type
article
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article

SIRT1 RegulatesFumonisin B1-Induced LMH Cell PANoptosisand Antagonism of Lycopene

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Mycorrhizal Fungi and Plant Interactions
article

SIRT1 RegulatesFumonisin B1-Induced LMH Cell PANoptosisand Antagonism of Lycopene

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Abstract

Mycotoxin contamination is a universal agricultural problem and a critical health issue. Fumonisin B1 (FB1) is one of the most toxic and extensive fumonisins that exist in various agro-products and foods. Lycopene (LYC), as a natural carotenoid, is becoming increasingly favored owing to its oxidation resistance. Here, we aim to explore the mechanism of FB1-induced hepatotoxicity and the antagonism of LYC. In this study, our findings indicated that FB1 induced mitochondrial structure damage and loss of mitochondrial function in chicken hepatocytes. Furthermore, FB1 upregulated the expression of PANoptosis-related signal molecules. FB1 also reduced the levels of SIRT1 and Ac-FOXO1 protein expression, which then inhibited mitophagy. However, LYC relieved these FB1-induced alterations. Most importantly, SIRT1 knockdown inhibited the protective effects of LYC in FB1-induced mitochondrial damage and PANoptosis. Our study provides evidence for the role of LYC in mycotoxin-induced chicken hepatocyte injury and points to SIRT1 as a potential target for liver protection.

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