Rosemary extract mitigates deoxynivalenol-induced intestinal inflammation in weaned piglets via activation of the Nrf2/HO-1 pathway and suppression of NF-κB/MAPK signaling

This study investigated the protective role of rosemary extract (RE) against intestinal inflammation induced by deoxynivalenol (DON) in weaned piglets. Sixty piglets were randomly allocated to three dietary treatments for a 21-day period: a basal diet (Control), a basal diet supplemented with 1.5 mg/kg DON (DON group), and a basal diet containing 200 mg/kg RE plus 1.5 mg/kg DON (RE + DON group). Dietary RE supplementation alleviated the negative impacts of DON on growth performance and organ indices (liver and spleen), while also improving DON-induced alterations in serum biochemical markers. RE effectively reduced intestinal oxidative stress, as evidenced by decreased concentrations of malondialdehyde (MDA) and reactive oxygen species (ROS), along with restored activities of glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), and superoxide dismutase (SOD) in the intestinal mucosa. Moreover, DON exposure increased the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and decreased anti-inflammatory cytokines (e.g., TGF-β, IL-10) in the mucosa, whereas RE supplementation significantly restored cytokine balance. At the molecular level, DON inhibited the Nrf2-Keap1 antioxidant pathway, while RE enhanced the expression of Nrf2, Keap1, and the downstream targets HO-1 and NQO1, thereby mitigating oxidative damage. Furthermore, RE suppressed the DON-induced activation of MAPK (ERK, p38, JNK) and NF-κB p65 signaling pathways, which contributed to the reduction of mucosal inflammation. In summary, RE attenuates DON-induced intestinal injury in weaned piglets by activating the Nrf2/HO-1 antioxidant pathway and inhibiting the MAPK/NF-κB inflammatory signaling cascade.

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