Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. The purpose of this study is to investigate whether CUR can reduce the damage of bovine mammary epithelial cells (MAC-T) induced by LPS and its underlying molecular mechanism. The MAC-T cell line was treated with different concentrations of LPS and CUR for 24 h. The results showed that CUR rescued the decrease of MAC-T cell viability and cell damage induced by LPS. At the same time, 10 µM CUR and 100 µg/mL LPS were used to treat the cells in the follow-up study. The results showed CUR treatment reduced the accumulation of reactive oxygen species (ROS), the expression of inflammatory cytokines (tumor necrosis factor-a (TNF-α), interleukin-8 (IL-8), IL-6 and IL-1β) and the rate of apoptosis induced by LPS. These effects were associated with the activation of the nuclear factor E2-related factor 2 (NFE2L2)-antioxidant response element (ARE) pathway coupled with inactivation of the nuclear factor-κB (NF-κB) inflammatory and caspase/Bcl2 apoptotic pathways.

Deoxynivalenol (DON) is a toxic secondary metabolite produced byFusarium graminearum. It is one of the most common feed contaminants that poses a serious threat to the health and performance of dairy cows. This study investigated the in vitro cytotoxicity of DON on bovine mammary epithelial cells (MAC‐T). DON at different concentrations (0.25, 0.3, 0.5, 0.8, 1 or 2 μg/ml) inhibited the growth of MAC‐T cells after 24 hr of exposure (p < .001). DON at 0.25 μg/ml increased lactate dehydrogenase (LDH) leakage (p < .05); decreased glutathione (GSH) levels (p < .001), total superoxide dismutase (T‐SOD) activity and total antioxidant capacity (T‐AOC;p < .01); and increased malondialdehyde (MDA) concentration (p < .01) in MAC‐T cells after 24 hr of exposure. We also observed that DON increased reactive oxygen species (ROS) levels in cells incubated for 9, 15 and 24 hr (p < .001). DON at 0.25 μg/ml triggered oxidative damage in MAC‐T cells. Furthermore, it induced an inflammatory response in the cells incubated for 9, 15 and 24 hr (p < .05) by increasing the mRNA expression levels of nuclear factor kappa B, myeloid differentiation factor 88 (MyD88), tumour necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), IL‐6, cyclooxygenase‐2 and IL‐8. We further examined the effect of DON on apoptosis. DON prevented normal proliferation of MAC‐T cells by blocked cell cycle progression in 24 hr (p < .001). In addition, the apoptosis rate measured using annexin V‐FITC significantly increased (p < .05) with increase in the mRNA expression level of Bax (p < .01) and increase in the Bax/Bcl‐2 ratio (p < .01) in cells incubated for 24 hr. In summary, DON exerts toxic effects in MAC‐T cells by causing oxidative stress, inducing an inflammatory response, affecting cell cycle and leading to apoptosis.

β-sitosterol, a natural plant steroid, has been shown to promote anti-inflammatory and antioxidant activities in the body. In this study, β-sitosterol was used to protect against lipopolysaccharide (LPS)-induced cell damage in bovine mammary epithelial cells, which are commonly studied as a cell model of mammary inflammatory response and lipogenesis. Results showed that treatment with a combination of LPS and β-sitosterol significantly reduced oxidative stress and inflammation, while increasing the expression of anti-apoptotic proteins and activating the hypoxia-inducible factor-1(HIF-1α)/mammalian target of rapamycin(mTOR) signaling pathway to inhibit apoptosis and improve lipid synthesis-related gene expression. Our finding suggests that β-sitosterol has the potential to alleviate inflammation in the mammary gland.

This study was conducted to examine the effects of supplementing brown seaweed by-products (BSB) in the diet of ruminants on ruminal fermentation characteristics, growth performance, endocrine response, and milk production in Holstein cows. In Experiment 1, the effects of different levels (0%, 2%, and 4% of basal diet as Control, 2% BSB, 4% BSB, respectively) of BSB were evaluated at 3, 6, 9, 12, and 24 h in vitro batch culture rumen fermentation. The pH tended to be higher for the higher level of BSB supplementation, with the pH at 12 h being significantly higher (p<0.05) than that of the control. The concentration of ammonia nitrogen was lower at 3, 9, 12, and 24 h incubation (p<0.05) compared with the control, and tended to be low at other incubation times. Volatile fatty acid concentration appeared to be minimally changed while lower values were observed with 4% BSB treatment at 24 h (p<0.05). In Experiment 2, effects of levels (0%, 2%, and 4%) of BSB on growth performance, endocrine responses and milk production were studied with Holstein dairy cows during transition. Dry matter intake, daily gain and feed efficiency were not affected by BSB supplementation. The concentration of plasma estrogen for the control, 2% BSB and 4% BSB after three months of pregnancy were 55.7, 94.1, and 72.3 pg/mL, respectively (p = 0.08). Although the differences of progesterone levels between BSB treatments and the control were minimal, the concentration in 4% BSB treatment increased to 157.7% compared with the initial level of the study. Triiodothyronine and thyroxine levels were also higher after both three months and eight months of pregnancy than the initial level at the beginning of the study. In addition, BSB treatments during one month after delivery did not affect daily milk yield and composition. In conclusion, the present results indicate that supplementation of BSB did not compromise ruminal fermentation, and animal performance at lower levels and hence may have potential to be used as a safe feed ingredient in dairy cows.

Zearalenone (ZEA) is a mycotoxin that is mainly produced by Fusarium fungi in food and feed. It causes many adverse effects on mammals, but there is little research on the effects of ZEA on intestinal mucosal immunity and intestinal flora in animals or humans. In this study, we aimed to explore the effects of short-term ZEA exposure on mucosal immunity and the microecological balance of the intestine. We found that the morphological structure of the intestinal mucosa in mice was severely destroyed after ZEA was administered by gavage for one week, and the mRNA expression levels of mucosal β-defensin, Mucin-1, Mucin-2, interleukin-1beta (IL-1β), and tumour necrosis factor-α (TNF-α) and secretory immunoglobulin A (sIgA) levels were significantly increased. In addition, the intestinal microflora was altered by ZEA. Our study showed that ZEA not only caused inflammation of the mucous membrane but also disturbed the microecological balance of the intestine in mice.