Plant-Derived Polyphenols as Nrf2 Activators to Counteract Oxidative Stress and Intestinal Toxicity Induced by Deoxynivalenol in Swine: An Emerging Research Direction

Abstract

The contamination of deoxynivalenol (DON) in feed is a global problem, which seriously threatens the productivity efficiency and welfare of farm animals and the food security of humans. Pig is the most sensitive species to DON, and is readily exposed to DON through its grain-enriched diet. The intestine serves as the first biological barrier to ingested mycotoxin, and is, therefore, the first target of DON. In the past decade, a growing amount of attention has been paid to plant-derived polyphenols as functional compounds against DON-induced oxidative stress and intestinal toxicity in pigs. In this review, we systematically updated the latest research progress in plant polyphenols detoxifying DON-induced intestinal toxicity in swine. We also discussed the potential underlying mechanism of action of polyphenols as Nrf2 activators in protecting against DON-induced enterotoxicity of swine. The output of this update points out an emerging research direction, as polyphenols have great potential to be developed as feed additives for swine to counteract DON-induced oxidative stress and intestinal toxicity.

Rehmannia glutinosa Polysaccharides: Optimization of the Decolorization Process and Antioxidant and Anti-Inflammatory Effects in LPS-Stimulated Porcine Intestinal Epithelial Cells

“…The Keap1-Nrf2 signaling pathway is a key regulator of resistance to OS. It not only serves as an important defense system against oxidative damage but is also a key enhancer of the body’s antioxidant capacity [ 39 ]. Under normal conditions, Nrf2 is anchored to the cytoplasm in an inactive state and shows low transcriptional activity.…”

Lauric acid reduces apoptosis by inhibiting FOXO3a-signaling in Deoxynivalenol-treated IPEC-J2 cells

“…DON is a mycotoxin that causes various symptoms such as anorexia, vomiting, and stunted growth, leading to poor health and economic loss [22]. The intestine is the first biological barrier to mycotoxins because it is the first target of exposure after consuming contaminated food [23,24]. Intestinal exposure to DON causes symptoms such as destruction of intestinal epithelial cells, impairment of integrity of intestinal barrier, destruction of tight junction protein structures, increased intestinal epithelial permeability, reduced nutrient absorption and transport efficiency, inflammation, and induction of apoptosis [25].…”

Insights into the intestinal toxicity of foodborne mycotoxins through gut microbiota: A comprehensive review

“…The nuclear factor erythroid 2‐related factor 2 (Nrf2) functions as a critical regulator of intracellular redox status, controlling the proliferation, differentiation, and apoptosis of intestinal cells, thus maintaining gut homeostasis (Hochmuth et al., 2011). Recent research has confirmed that exposure to various mycotoxins, including AFB 1 (Zhang, Zhang, Li, Xu et al., 2022), FB 1 (Chen, Abdallah, et al., 2022), OTA (Tao et al., 2018), DON (Chen, Huang, et al., 2022; Zhu et al., 2023), ZEN (Cheng et al., 2019), or T‐2 (Li, Wang, et al., 2022), can stimulate the intestinal tract, leading to oxidative stress. Consequently, this triggers an increase in reactive oxygen species (ROS) and malondialdehyde levels in the intestinal tract while concurrently reducing key oxidative stress indicators, such as superoxide dismutase, catalase, and glutathione.…”