Lauric acid reduces apoptosis by inhibiting FOXO3a-signaling in Deoxynivalenol-treated IPEC-J2 cells

Na Yeon Kim1, Sang In Lee1,*
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1Department of Animal Biotechnology, Kyungpook National University,, Sangju 37224, Korea.
*Corresponding Author: Sang In Lee, Department of Animal Biotechnology, Kyungpook National University,, Sangju 37224, Korea, Republic of. Phone: 82-54-530-1943. E-mail:

© Copyright 2023 Korean Society of Animal Science and Technology. This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Deoxynivalenol (DON) is the most common mycotoxin contaminant of food or feed worldwide and causes disease in animals. Lauric acid (LA) is a medium-chain fatty acid useful for barrier functions such as antimicrobial activity in the intestine of monogastric animals. However, the molecular mechanisms by which lauric acid exerts its effects on the deoxynivalenol-exposed small intestine have not been studied. We used an intestinal porcine epithelial cell line (IPEC-J2) as an <italic>in vitro</italic> model to explore the molecular mechanism of lauric acid in alleviating deoxynivalenol-induced damage. We found that lauric acid reversed deoxynivalenol-induced reduction in cell viability. Our qRT-PCR results indicated that lauric acid alleviated deoxynivalenol-induced apoptosis through Annexin-V. Additionally, immunofluorescence and Western blotting showed that lauric acid attenuated deoxynivalenol-induced Forkhead box O3 (FOXO3a) translocation. These results suggest that lauric acid attenuates Forkhead box O3 translocation in the small intestine damaged by deoxynivalenol, thereby reducing apoptosis. In conclusion, this study found that lauric acid alleviates deoxynivalenol-induced damage in intestinal porcine epithelial cell line through various molecular mechanisms.

Keywords: IPEC-J2 cells; Deoxynivalenol; Lauric acid; Apoptosis; Foxo3a