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With the purpose to explore the relationship between deoxynivalenol (DON)-induced apoptosis and autophagy and provide mechanistic explanations for the toxic effects of DON on IPEC-J2 cells, we determined the cell viability, cell morphology, apoptosis, and autophagy by using autophagy inhibitor 3-methyladenine (3-MA), PI3K pathway inhibitor LY294002, and activator 740Y-P. It turned out that 3-MA was able to attenuate the reduction of cell viability induced by DON. Moreover, 3-MA was capable of upregulating the expression of DON-induced autophagic protein p62 and downregulating the expressions of DON-induced autophagic protein LC3-II and apoptotic protein Bax, suggesting that autophagy is a driving mechanism for this apoptotic induction. The results of Annexin V-FITC/PI double staining indicated that DON could induce apoptosis by inhibiting the PI3K-AKT-mTOR signaling pathway. Subsequently, it was further confirmed by Western blot analysis that DON significantly decreased expressions of P-AKT/AKT, p-mTOR/mTOR, and autophagic protein p62, and increased expression of autophagy-related protein LC3-II, suggesting that DON triggered autophagy by inhibiting the PI3K-AKT-mTOR signaling pathway. To conclude, these data reveal that DON may induce cytotoxicity and apoptosis through the activation of autophagy by suppressing the PI3K-AKT-mTOR signaling pathway. This study provides new insights into the mechanisms by which DON incurs cytotoxic effects.

Deoxynivalenol-Induced Cytotoxicity and Apoptosis in IPEC-J2 Cells Through the Activation of Autophagy by Inhibiting PI3K-AKT-mTOR Signaling Pathway