Lipopolysaccharide (LPS) is an endotoxin that induces immune and inflammatory responses in the rumen epithelium of dairy cows. It is well-known that flavonoid phloretin (PT) exhibits anti-oxidative, anti-inflammatory and antibacterial activity. The aim of this research was to explore whether PT could decrease LPS-induced damage to bovine rumen epithelial cells (BRECs) and its molecular mechanisms of potential protective efficacy. BRECs were pretreated with PT for 2 h and then stimulated with LPS for the assessment of various response indicators. The results showed that 100 µM PT had no significant effect on the viability of 10 µg/mL LPS-induced BRECs, and this dose was used in follow-up studies. The results showed that PT pre-relieved the decline in LPS-induced antioxidant indicators (T-AOC and GSH-PX). PT pretreatment resulted in decreased interleukin-1β (IL-1β), IL-6, IL-8, tumor necrosis factor-α (TNF-α) and chemokines (CCL2, CCL5, CCL20) expression. The underlying mechanisms explored reveal that PT may contribute to inflammatory responses by regulating Toll-like receptor 4 (TLR4), nuclear transcription factor-κB p65 (NF-κB p65), and ERK1/2 (p42/44) signaling pathways. Moreover, further studies found that LPS-induced BRECs showed decreased expression of claudin-related genes (ZO-1, Occludin); these were attenuated by pretreatment with PT. These results suggest that PT enhances the antioxidant properties of BRECs during inflammation, reduces gene expression of pro-inflammatory cytokines and chemokines, and enhances barrier function. Overall, the results suggest that PT (at least in vitro) offers some protective effect against LPS-induced ruminal epithelial inflammation. Further in vivo studies should be conducted to identify strategies for the prevention and amelioration of short acute rumen acidosis (SARA) in dairy cows using PT.

This study was conducted to investigate the effects of two mycotoxin detoxifications on laying hens. A total of 360 70-week-old Hy-Line Brown laying hens were randomly divided into 1 of the 4 dietary treatment groups, with 6 replicates per group and 15 hens per replicate. The laying hens of the four treatments were fed with a basal diet (CON), a diet with naturally low-level mycotoxin contaminated corn (the levels of AFB₁, ZEA, and DON in the corn of the CON group were 1.68 μg/kg, 42.75 μg/kg, and 585.40 μg/kg, respectively), replacing 73% of the corn in CON (MC), the MC diet with 1 g/kg modified silica-aluminate mycotoxin adsorbent (MA), and the MC diet with 1 g/kg mycotoxin degrading enzyme and bacteria complexes degradation agent (MD), respectively. Liver tissue and serum samples were extracted at the end of the trial to assess the antioxidant status and hepatic injury biomarkers. The experimental data were preliminarily interpreted in Excel and then analyzed by one-way ANOVA using SPSS, version 25 (SPSS Inc., Chicago, IL, USA). The results showed that compared to the CON, the MC group had decreased laying rate (p < 0.05), ferric reducing antioxidant potential in serum (p < 0.05), and reduced glutathione (GSH) content in the liver, and increased feed/egg ratio, serum alanine aminotransferase (ALT) activity, and malondialdehyde (MDA) content. Compared to the MC group, feed/egg ratio and serum ALT activity in the MA group and MD group decreased (p < 0.05), while serum GSH content and superoxide dismutase activity in the liver of the MA and MD groups increased. The liver glutathione peroxidase activity and the egg yolk percentage in the MA group decreased (p < 0.05) compared to the MC group. Histopathological alterations in liver tissues induced by mycotoxin included vacuolar degeneration, hepatocyte necrosis and disintegration, inflammatory cell infiltration, and enlarged hepatic sinuses. In short, both MA and MD were effective in mitigating the combined effects of low-level mycotoxins on laying hen performance, antioxidant capacity and liver damage.