stilbenes and deoxynivalenol

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.

Topics: Animals; Antioxidants; Cattle; Cell Survival; Epithelial Cells; Kelch-Like ECH-Associated Protein 1; NF-E2-Related Factor 2; Oxidative Stress; Reactive Oxygen Species; Stilbenes; Superoxide Dismutase; Trichothecenes

Contamination of food/feedstuffs by mycotoxins is a serious problem worldwide, causing severe economic losses and serious health problems in animals/humans. Deoxynivalenol (DON) is a major mycotoxin contaminant and is known to impair intestinal barrier function. Grapes and red wine are rich in polyphenols, such as resveratrol (RES), which has striking antioxidant and anti-inflammatory activities. RES is a food-derived component; therefore, it may be simultaneously present with DON in the gastrointestinal tract. The aim of this study was to explore in vitro protective effects of RES against DON-induced intestinal damage. The results showed that RES could protect DON-induced bacteria translocation because of enhanced of intestinal barrier function by restoring the DON-induced decrease in transepithelial electrical resistance and increase in paracellular permeability. Further mechanistic studies demonstrated that RES protects against DON-induced barrier dysfunction by promoting the assembly of claudin-4 in the tight junction complex. This is probably mediated through modulation of IL-6 and IL-8 secretion via mitogen-activated protein kinase-dependent pathways. Our results imply that RES can protect against DON-induced intestinal damage and that RES may be used as a novel dietary intervention strategy to reduce DON toxicity in animals/humans.

Topics: Animals; Bacterial Translocation; Cell Line; Cytokines; Inflammation Mediators; Intestinal Mucosa; Intestines; Resveratrol; Stilbenes; Swine; Trichothecenes

Exposure to mycotoxins through dietary food intake involves a highly complex scenario where co-contamination of different mycotoxins has been frequently demonstrated. On the other hand, the effect of the interaction of mycotoxins with other generally considered beneficial food components, as the antioxidants, has been scarcely studied. The main goal of the present work was to assess the cytotoxic effects on Caco-2 cells of the mycotoxins deoxynivalenol (DON) and ochratoxin A (OTA), alone or combined, and to explore potential protective effects of resveratrol (RES), an antioxidant frequently found in wine. In parallel, reactive oxygen species (ROS) production has also been studied as a first approach to understand the underlying mechanism of cytotoxicity. Results indicate a higher toxic effect of the mycotoxins when they are co-exposed. This increase in cytotoxicity was not accompanied by an increase in ROS production. The co-exposure of OTA or DON with RES did not result in a decrease in cytotoxicity; on the contrary, it resulted in increased cytotoxicity not associated with an increase in ROS production.

Topics: Antioxidants; Caco-2 Cells; Cell Survival; Drug Interactions; Humans; Ochratoxins; Reactive Oxygen Species; Resveratrol; Stilbenes; Trichothecenes

The aim of this in vitro study was to examine the release of progesterone by porcine ovarian granulosa cells (GCs) after exposure to toxic concentrations of deoxynivalenol (DON), resveratrol (RSV), and their combination (DON with RSV). Ovarian granulosa cells were incubated without (control) or with treatments of natural substances at various doses for 24 h: RSV (10, 30 and 50 μg/mL) / DON (2000, 3000 and 5000 ng/mL), and their combination (10 μg/mL of RSV with 2000 ng/mL of DON; 30 μg/mL of RSV with 3000 ng/mL of DON; 50 μg/mL of RSV with 5000 ng/mL of DON). Progesterone was determined by radioimmunoassay (RIA). Progesterone release was significantly (P < 0.05) stimulated by RSV at the doses 50 μg/mL but not at 30 and 10 μg/mL and by DON treatment at all used doses (2000, 3000 and 5000 ng/mL). RSV in combination with DON stimulated significantly (P < 0.05) the progesterone release by GCs at the highest doses (50 μg/mL of RSV with 5000 ng/mL of DON). On the other hand, the stimulatory effect of RSV in combination with DON was significantly (P < 0.05) lower in comparison with alone DON effect. In conclusion, our results indicate, (1) the dose-depended stimulatory effects of RSV, DON and combination of RSV with DON on release of steroid hormone progesterone and (2) reduction of the stimulatory effect of DON by RSV. Our in vitro results suggest that reproductive toxicity of animals induced by a mycotoxin - deoxynivalenol can be inhibited by a protective natural substance - resveratrol.

Topics: Animals; Female; Reproduction; Resveratrol; Stilbenes; Swine; Trichothecenes