Unraveling the Nrf2-ARE Signaling Pathway in DF-1 Cells: Insights into T-2 Toxin-Induced Oxidative Stress Regulation

Abstract

Abstract T-2 toxin (T2) poses a major threat to the health and productivity of animals and livestock. The induction of oxidative stress by T2 has been identified as a central factor in cellular damage. The Nrf2-ARE signaling pathway represents a crucial regulatory mechanism that protects cells from oxidative stress, with nuclear factor E2 related factor 2 (Nrf2) serving as a vital component in this defense. To date, there has been a lack of research on the role of Nrf2 in mediating the effects of T2-induced oxidative stress in broilers. The present study aimed to investigate the regulatory mechanism of Nrf2 protein derived from broilers against T2-induced oxidative damage by constructing Nrf2 overexpression and knockdown DF-1 cell lines. Normal DF-1 cells, Nrf2 overexpressing cells, and Nrf2 knockdown cells were subjected to treatment with 50nM T2 for 24 hours. Results showed that an increase in Nrf2 protein levels was associated with a decrease in oxidative stress in DF-1 cells (P < 0.05) and an upregulation of antioxidant factor mRNA and protein expression. Conversely, downregulation of Nrf2 protein resulted in the opposite outcomes. This study provides valuable insights into the potential treatment of oxidative stress-related diseases in livestock and poultry.