Avian pathogenic Escherichia coli ( APEC ) is the causative agent of avian colibacillosis. Baicalin ( BA ) possesses multiple pharmacological effects, but the mechanism underlying its activity in APEC-induced intestinal injury remains unknown. This study aims to investigate the protective effects and possible mechanism of BA against APEC-induced intestinal injury. Sixty 1-day-old chicks were randomly divided into 4 groups: the control group (basal diet), E. coli group (basal diet), BAI10 group (10 mg/kg BA), and BAI20 group (20 mg/kg BA). After pretreatment with BA for 15 d and subsequent induction of APEC infection by pectoralis injection, the ileum was collected and analyzed. The results showed that BA-pretreatment demonstrated an alleviation of chicks in diarrhea rate, mortality, and histopathological changes in intestinal tissues after APEC infection. Additionally, following APEC infection, BA improved the intestinal barrier by elevating zona occludens ( ZO )s (ZO-1, 2, 3), Claudins (Claudin1, 2, 3), Occludin, avian β-defensin ( AvBD )s (AvBD1, 2, 4), lysozyme ( Lyz ) mRNA levels and ZO-1, Claudin1, and Occludin protein levels. Besides, the activities of total superoxide dismutase ( T-SOD ), catalase ( CAT ), and glutathione peroxidase ( GSH-Px ) and the SOD-1 and CAT mRNA levels and SOD-1 protein level were elevated by BA pretreatment. BA pretreatment also decreased the malondialdehyde ( MDA ) content, heme oxygenase-1 ( HO-1 ) and NADH quinone oxidoreductase 1 ( NQO1 ) mRNA levels, and HO-1 protein level after APEC infection. BA alleviated the APEC-induced inflammatory response, including downregulating the mRNA levels of proinflammatory cytokines (tumor necrosis factor-α ( TNF-α ), interleukin [ IL ]-1β, IL-6, IL-8) and upregulating the mRNA levels of anti-inflammatory cytokines (IL-4, IL-10, IL-13, transforming growth factor-β [ TGF-β ]). Furthermore, BA decreased the mRNA and protein levels of phosphatidylinositol 3 kinase ( PI3K ), protein kinase B ( AKT ), and nuclear factor kappa-B ( NF-κB ) as well as the expression of the phosphorylated forms of these proteins after APEC infection. Collectively, our findings indicate that BA exerts a protective effect against APEC-induced intestinal injury in chicks by inhibiting the PI3K/AKT-mediated NF-κB pathway, suggesting that BA may be a potential therapeutic approach for avian colibacillosis.

Cadmium (Cd) is a toxic heavy metal that can accumulate in the liver of animals, damaging liver function. Inflammation and oxidative stress are considered primary causes of Cd-induced liver damage. Selenium (Se) is an antioxidant and can resist the detrimental impacts of Cd on the liver. To elucidate the antagonism of Se on Cd against hepatocyte injury and its mechanism, duck embryo hepatocytes were treated with Cd (4 μM) and/or Se (0.4 μM) for 24 h. Then, the hepatocyte viability, oxidative stress and inflammatory status were assessed. The findings manifested that the accumulation of reactive oxygen species (ROS) and the levels of pro-inflammatory factors were elevated in the Cd group. Simultaneously, immunofluorescence staining revealed that the interaction between NOD-like receptor pyran domain containing 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) was enhanced, the movement of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm was increased and the inflammatory response was further amplified. Nevertheless, the addition of Se relieved the above-mentioned effects, thereby alleviating cellular oxidative stress and inflammation. Collectively, the results suggested that Se could mitigate Cd-stimulated oxidative stress and inflammation in hepatocytes, which might be correlated with the NLRP3 inflammasome and HMGB1/nuclear factor-κB (NF-κB) signaling pathway.

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Avian pathogenic E. coli (APEC) is typically the cause of avian colibacillosis, which can result in oxidative stress, inflammation, and intestinal damage (APEC). Luteolin, in the form of glycosylation flavone, has potent anti-inflammatory and anti-oxidative properties. However, its effects on APEC-induced intestinal oxidative stress and NF-κB-mediated inflammation in chicks remains poorly understood. After hatching, one-day-old chicks were stochastically assigned to four groups: a control group (basic diet), an E. coli group (basic diet) and L10 and L20 groups (with a dry matter of luteolin diet 10 mg/kg and 20 mg/kg, respectively), with fifteen chicks in each group and one repeat per group. They were pretreated for thirteen days. The body weight, mortality, histopathological changes in the ileum, antioxidant status, and the mRNA and protein-expression levels of factors associated with the HMGB1/TLR4/NF-κB signal axis of the chicks were measured. The results showed that luteolin treatment decreased the mRNA and protein-expression level of the related factors of HMGB1/TLR4/NF-κB signal axis in the ileum, reduced inflammation, increased antioxidant enzyme activity, and reduced intestinal injury. Collectively, luteolin alleviated APEC-induced intestinal damage by means of hindering the HMGB1/TLR4/NF-κB signal axis, which suggests that luteolin could be a good method for the prevention and treatment of avian colibacillosis.