Curcumin Attenuates Fumonisin B1-Induced PK-15 Cell Apoptosis by Upregulating miR-1249 Expression to Inhibit the IRE1/MKK7/JNK/CASPASE3 Signaling Pathway.

Abstract

Fumonisin B1 (FB1) is an important toxin which poses global concerns in terms of food safety. Curcumin (Cur), a natural polyphenolic compound, has strong antioxidant and anti-inflammatory effects. Meanwhile, the mechanisms underlying the mitigation of FB1-induced toxicity by Cur are not fully understood, limiting its potential application as a novel feed additive to prevent FB1 toxicity. In this study, porcine kidney cells (PK-15) were used as an experimental model, utilizing mRNA and miRNA transcriptome technologies. The results revealed that Cur upregulated miR-1249 and inhibited the target gene Ern1 in the PK-15 cells, thereby suppressing the IRE1/MKK7/JNK/CASPASE3 endoplasmic reticulum (ER) stress pathway and alleviating FB1-induced cell apoptosis. Cell transfection experiments confirmed that Cur effectively attenuated the apoptosis induced by ER stress following transfection with a miR-1249 inhibitor. Similarly, transfection with a miR-1249 mimic alleviated the ER stress and FB1-induced PK-15 cell apoptosis. These findings reveal that Cur mitigates FB1-induced ER stress and significantly reduces apoptotic damage in porcine kidney cells.