Pterostilbene inhibits deoxynivalenol-induced oxidative stress and inflammatory response in bovine mammary epithelial cells.

Abstract More and more studies have showed that tricothecene mycotoxin, deoxynivalenol (DON) caused cytotoxicity in mammary alveolar cells-large T antigen cells (MAC-T). Therefore, research on reducing the cytotoxicity of DON has gradually attracted attention. In this study, we aim to explore the potential of pterostilbene (PTE) to protect MAC-T cells from DON-induced oxidative stress and inflammatory response. MAC-T cells were treated with 0.25 μg/mL DON or 2.0504 μg/mL PTE or 0.25 μg/mL DON and 2.0504 μg/mL PTE together, incubated for 9 h. PTE effectively improved cell viability, cell proliferation and total antioxidant capacity (T-AOC), reduced reactive oxygen species (ROS) production and malondialdehyde (MDA), and improved glutathione (GSH) depletion. Moreover, PTE effectively regulated the mRNA levels of nuclear factor erythroid-2-related factor 2 (Nrf2), kelch-like ech-associated protein 1 (Keap1), superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2). PTE significantly inhibited nuclear factor kappa-B P65 (NF-κB P65), nuclear factor kappa-B P50 (NF-κB P50), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) mRNA levels in DON-induced MAC-T cells. PTE also significantly reduced inducible nitric oxide synthase (iNOS) and nitric oxide (NO) levels in DON-induced MAC-T cells. Additionally, ELISA revealed that PTE inhibited the expression of tumor necrosis factor-α (TNF-α) and IL-6 proteins produced in DON-induced MAC-T cells. These findings together provided strong evidence to support that PTE can effectively alleviate the damage to cells caused by DON, and it may be used as an effective anti-inflammatory and antioxidant to prevent the damage of mycotoxins to the animal body.