Fumonisin B1 induces oxidative stress, inflammation and necroptosis in IPEC-J2 cells.

Abstract

Fumonisin B1 (FB1), an important mycotoxin, poses a significant threat to public health and livestock production due to its widespread contamination. Furthermore, the gastrointestinal tract is particularly vulnerable to FB1 exposure given its frequent contamination of staple crops such as corn. Although necroptosis has been recognized as a critical mechanism underlying intestinal damage caused by certain environmental toxins, whether FB1 specifically triggers necroptosis in intestinal epithelial cells remains to be fully elucidated. In this study, the intestinal porcine epithelial cell line-J2 (IPEC-J2) was employed as an in vitro model to study the intestinal cells injury caused by FB1 and the underlying mechanisms. By measuring IPEC-J2 cell viability, intracellular reactive oxygen species, gene levels, and protein levels, it was found that FB1 dose-dependent induced IPFC-J2 cell injury, oxidative stress, and inflammation. Meanwhile, FB1 significantly increased the expression of necroptosis-related genes and proteins in IPEC-J2 cells, indicating that FB1 induced the occurrence of necroptosis. In summary, the results demonstrated FB1 can induce oxidative stress, inflammation and necroptosis in IPEC-J2 cells.