Zearalenone (ZEA)-Induced intestinal epithelial cell (IPEC-J2) damage: Role of oxidative stress and inflammation

This study explored the molecular mechanisms underlying zearalenone (ZEA)-induced damage in porcine intestinal epithelial cells (IPEC-J2), focusing on oxidative stress and inflammatory pathways. Cells were exposed to ZEA (0-100 μM), and assessments included cell viability (CCK-8 assay), oxidative stress markers (ROS, SOD, CAT, GSH-Px, MDA), inflammatory cytokines (ELISA, RT-qPCR), and Nrf2/NF-κB pathway proteins (Western blot). RESULTS: ZEA dose-dependently reduced viability, elevated ROS and MDA, and suppressed antioxidant enzyme activities. It also upregulated TNF-α, IL-1β, IL-6, and IL-8 expression. Mechanistically, ZEA inhibited Nrf2 nuclear translocation and downstream antioxidant genes (HO-1, NQO1) while promoting NF-κB p65 activation. Notably, NAC pretreatment alleviated ZEA-induced inflammation, and BAY11-7082 reduced oxidative stress, indicating pathway crosstalk. CONCLUSIONS: ZEA disrupts intestinal homeostasis by suppressing Nrf2-mediated antioxidant defense and triggering NF-κB-driven inflammation. These insights enhance understanding of ZEA toxicity and support the development of targeted protective strategies.