Protection of Porcine Intestinal-Epithelial Cells from Deoxynivalenol-Induced Damage by Resveratrol via the Nrf2 Signaling Pathway.

Deoxynivalenol (DON), a common mycotoxin, usually induces oxidative stress and affects the intestinal health of humans and animals. This study investigated the protective effect of resveratrol (RES), a natural antioxidant, on alleviating the cytotoxicity induced by DON in the porcine intestinal-epithelial cell line (IPEC-J2). Cells were incubated with RES for 24 h and then exposed to DON for another 24 h. Cell viability, proliferation, apoptosis, and oxidative-stress indicators were determined. In comparison with DON-only-treated cells, pretreatment with RES (15 μM) increased the cell viability (79.74 ± 2.02 vs 90.98 ± 2.66%, P < 0.01), improved proliferation (EdU-positive cells, 26.42 ± 1.12 vs 32.05 ± 0.78%, P < 0.01), decreased accumulation of intracellular reactive oxygen species (ROS, 1.68 ± 0.05 vs 1.29 ± 0.06, P < 0.01), stabilized mitochondrial-membrane potential (MMP, 8.98 ± 1.40 vs 2.29 ± 0.76, P < 0.001), and prevented apoptosis induced by DON (13.91 ± 1.20 vs 6.83 ± 0.52%, P < 0.01). RES activated the Nrf2 signaling pathway, and transfection with Nrf2 siRNA abrogated the protection of RES against DON-induced cytotoxicity, accumulation of intracellular ROS, and mitochondria-dependent apoptosis. Collectively, RES protects IPEC-J2 cells against DON-induced damage at least partly via the Nrf2 signaling pathway.