Chlorogenic acid alleviates IPEC-J2 pyroptosis induced by deoxynivalenol through inhibiting the activation of NF-κB/NLRP3/Capase-1 pathway

Abstract Background Deoxynivalenol (DON) is a severely polluted mycotoxins in feed ingredients, and methods for reducing its toxicity have become a significant direction of research. Chlorogenic acid (CGA) in some plants is an active polyphenol with anti-inflammatory and antioxidant properties and a protective effect on animal intestinal health. The effects of CGA on DON-induced pyroptosis of the intestinal porcine epithelial cell line-J2 (IPEC-J2) and its potential mechanism were explored in this study. Results The results indicated that exposure to DON at 2500 ng/mL significantly increased the mortality of IPEC-J2 cells, accompanied by typical pyroptosis features, including breakage of cellular DNA, damage to cell membrane integrity, and an increase in the extracellular concentration of positive ions (Ca2+ and K+) and pro-inflammatory cytokines (IL-1β and IL-18). Nevertheless, DON-induced pyroptosis was alleviated by CGA. Additionally, the exposure of DON promoted the mRNA expression of initiating signaling factors relevant to pyroptosis (including TNF, MDP, NOD2, TLR4, and NF-κB), enhanced the mRNA and protein levels of activation signaling factors (including NLRP3, ASC, Caspase-1, and GSDMD), and increased the level of ROS. Among them, the NF-κB/ROS/NLRP3/Capase-1 pathway was identified as the key factor in the dual-signaling pathway. Our findings suggest that CGA pretreatment simultaneously inhibits the activation of both the initiating and activation signals related to pyroptosis. Conclusion In short, CGA can alleviate DON-induced pyroptosis of IPEC-J2 cells through inhibiting the activation of NF-κB/ROS/NLRP3/Capase-1 pathway.