Protective effects of melatonin on deoxynivalenol-induced oxidative stress and autophagy in IPEC-J2 cells

This study explored protective effects of melatonin (MEL) on deoxynivalenol (DON)-induced toxicity in porcine jejunum epithelial cells (IPEC-J2). Cells were preexposed to MEL and then exposed to DON to detect cell viability, apoptosis, and oxidative stress indicators. Compared to DON treatment, pretreatment with MEL significantly increased cell proliferation. (P < 0.01), intracellular catalase (CAT) and superoxide dismutase (SOD) levels (P < 0.05), decreased apoptosis and oxidative stress, and significantly attenuated the inflammatory response. RNA-seq analysis revealed that MEL protects IPEC-J2 from the adverse effects of DON by affecting the expression of tight junction and autophagy pathway-related genes. Similarly, further experiments revealed that MEL partly prevented DON-induced disruption of intestinal barrier function and decreased autophagy induced by DON via activation of the AKT/mTOR pathway. In conclusion, these results demonstrated the preventive properties of MEL against DON-induced cell damage by activating the antioxidant system and Inhibition of autophagy.

Automated summary

This study investigated the protective effects of melatonin (MEL) against deoxynivalenol (DON)-induced toxicity in porcine jejunum epithelial cells (IPEC-J2). The results showed that pretreatment with MEL significantly increased cell proliferation, decreased apoptosis and oxidative stress, and attenuated the inflammatory response caused by DON exposure. RNA-seq analysis revealed that MEL protects IPEC-J2 cells from DON toxicity by regulating the expression of genes related to tight junctions and autophagy pathways. Additionally, MEL partly prevented DON-induced disruption of intestinal barrier function and decreased autophagy by activating the AKT/mTOR pathway.