To explore the protective role of hydrogen gas (H2) on oxidative damage and apoptosis in intestinal porcine epithelial cells (IPEC-J2) induced by deoxynivalenol (DON), cells were assigned to four treatment groups, including control, 5 μM DON, H2-saturated medium, and 5 μM DON + H2-saturated medium treatments. After 12 h of different treatments, the cell viability, biomarkers of cell redox states, and gene expression of antioxidant enzymes and apoptosis were observed and detected. Furthermore, caspase-3 and Bax protein expressions were measured by Western blot analysis. Our results demonstrated that the 5 μM DON significantly caused cytotoxicity to IPEC-J2 cells by reducing cell viability and increasing lactate dehydrogenase release in culture supernatants. Moreover, DON treatments significantly increased levels of 8-hydroxy-2'-deoxyguanosine, 3-nitrotyrosine, and malonaldehyde; however, they decreased total superoxide dismutase and catalase activities and downregulated messenger RNA (mRNA) expression related to antioxidant enzymes in cells. The 5 μM DON treatment also downregulated Bcl-2 expression and upregulated caspase-3 and Bax expression. However, the H2-saturated medium significantly improved cell growth status and reversed the change of redox states and expression of genes and proteins related to apoptosis induced by DON in IPEC-J2 cells. In conclusion, H2 could protect IPEC-J2 cells from DON-induced oxidative damage and apoptosis in vitro.
Keywords: IPEC-J2; apoptosis; deoxynivalenol; hydrogen gas; oxidative damage.