Alleviation effect of taxifolin on diquat-induced damage to porcine intestinal epithelial cells

Oxidative stress is considered to be a major cause of numerous intestinal diseases, and taxifolin (TA) possesses a variety of pharmacological properties that promote health and prevent disease. This study intends to determine the ability of TA to alleviate oxidative stress induced by diquat (DIQ) in porcine intestinal epithelial cells (IPEC-J2 cells). After being pretreated with 150 μM TA for 24 h, IPEC-J2 cells were treated with 0.5 mM DIQ for 6 h to cause oxidative stress. The results demonstrated that TA pretreatment increased cell viability and proliferation, significantly inhibited the DIQ-induced reductions in cell proliferation and cell viability, and ameliorated the intestinal barrier by up-regulating the expression levels of Claudin1 and Occludin. Furthermore, TA pretreatment weakened the DIQ-induced inflammatory response through reducing the gene expression of proinflammatory factors (IL-6 and IL-8) and increasing the antioxidant gene expression level, possibly through activating the Nrf2 signaling pathway. Taken together, these findings demonstrate that TA is a potent antioxidant that attenuates cytotoxicity and inflammation, protects cellular barrier integrity, and improves antioxidant function in DIQ-stimulated IPEC-J2 cells. This research explores the role of TA in mitigating intestinal oxidative stress damage and its potential as an eco-friendly feed additive in pig farming.

Diquat; IPEC-J2 cells; Oxidative stress; Taxifolin.