This study investigated the effects of dietary sodium butyrate (SB) supplementation, provided as a specially coated product, on growth performance, intestinal development, morphological structure and function in broilers. In total, 720 one-day-old Arbor Acres male broilers were randomly allocated into six treatment groups with six replicates each and then fed basal diets (control) supplemented with 0, 200, 400, 800 or 1000 mg/kg of SB or with antibiotics (100 mg/kg aureomycin and 20 mg/kg colistin sulfate). The growth trial lasted for 42 days. No differences (P>0.05) in growth performance were detected between groups during the grower period (1–21 d) or over the total (1–42 d) trial period, whereas the addition of SB improved the intestinal structure by stimulating (P<0.05) goblet cells on jejunal and ileal villi accompanied by a trend towards increased (Pdiets<0.10) ileal villus height. In addition, more inerratic leaf-shaped villi and mucus secretion and significantly fewer erosions were demonstrated by scanning electron microscopy. Apart from decreased (P<0.05) malondialdehyde (MDA) in the ileal mucosa at 21 d of age, supplemental SB at higher doses (800 mg/kg) led to greater (P<0.05) total antioxidant capacity and depressed (P<0.05) MDA concentrations in the jejunal mucosa. Birds fed with 400 mg/kg and 800 mg/kg SB had higher (P<0.05) acetic acid concentrations at 42 d and higher butyric acid at 21 d in the jejunum chyme. Morever, chicks fed SB diet were found to have higher concentrations of butyric acid (P<0.05) in the ileal chyme. SB additions at 400 mg/kg displayed higher Firmicutes and Proteobacteria levels, while a higher (P<0.05) relative abundance of Bacteroidetes was observed at 800 mg/kg. Furthermore, we found a striking decrease in Enterobacteriaceae and increases in Lachnospiraceae and Rikenellaceae in the cecal lumen of birds fed 800 mg/kg SB as well as a higher proportion of Ruminococcaceae and a noticeable reduction (P<0.05) of Lactobacillaceae in birds treated with 400 mg/kg SB. Taken together, our results support the importance of SB in improving the intestinal development, morphological structure and biological functions of broilers through modulation of the microbial community, which seems to be optimized for gut health at higher doses (800 mg/kg) of SB.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of intestinal mucosa and submucosa, characterized by the disruption of the intestinal epithelial barrier, increased production of inflammatory mediators, and excessive tissue injury. Intestinal epithelial cells, as well as microvascular endothelial cells, play important roles in IBD. To study the potential effects of kaempferol in IBD progress, we established a novel epithelial−endothelial cells coculture model to investigate the intestinal inflammation and barrier function. Data demonstrated an obvious increased transepithelial electrical resistance (TEER) (1222 ± 60.40 Ω cm 2 vs 1371 ± 38.77 Ω cm 2 ), decreased flux of FITC (180.8 ± 20.06 μg/mL vs 136.7 ± 14.78 μg/mL), and up-regulated occludin and claudin-2 expression in Caco-2 that was specifically cocultured with endothelial cells. Meanwhile, 80 μM kaempferol alleviated the drop of TEER, the increase of FITC flux, and the overexpression of interleukin-8 (IL-8) induced by 1 μg/mL lipopolysaccharide (LPS). Additionally, kaempferol also ameliorated the LPS-induced decrease of protein expression of zonula occludens-1 (ZO-1), occludin, and claudin-2, together with the inhibited protein expressions of the phosphorylation level of NF-κB and I-κB induced by LPS. Our results suggest that kaempferol alleviates the IL-8 secretion and barrier dysfunction of the Caco-2 monolayer in the LPS-induced epithelial−endothelial coculture model via inhibiting the NF-κB signaling pathway activation.

This study was conducted to evaluate the effects of quercetin on the antioxidant ability, intestinal barrier functions, and cecal microbiota in broiler chickens fed with oxidized soya oil. Four hundred eighty male Arbor Acres broilers were randomly assigned to 5 treatments, each involving 8 cages (12 birds per cage). The treatment groups were as follows: the control group, birds fed with basal diets containing oxidized oil, and birds fed with basal diets containing oxidized oil and supplemented with 200 ppm of quercetin, 400 ppm of quercetin, and 800 ppm of quercetin. The results showed that dietary supplementation with quercetin at a dose of 400 ppm or 800 ppm alleviated the increased serum malondialdehyde ( MDA ) level induced by oxidized oil on day 11 ( P = 0.005) and reversed the increased MDA level in the mucosa on day 11 ( P = 0.021). Quercetin significantly upregulated the transcription of nuclear factor erythroid 2–related factor 2 ( Nrf2 ) and its downstream genes such as catalase ( P < 0.001), superoxide dismutase 1 ( P < 0.001), glutathione peroxidase 2 ( P = 0.018), heme oxygenase-1 ( HO-1 ) ( P = 0.0), and thioredoxin ( P = 0.002) and reversed the mRNA expression of HO-1 ( P = 0.007) in the ileal mucosa. Tight junction protein 1 was only downregulated by oxidized oil ( P = 0.013). In addition, quercetin (800 ppm) alleviated the decreased mRNA expression of mucin 2 ( MUC2 ), which contributed to the intestinal chemical barrier ( P = 0.039). The supplemental dose of 400 ppm of quercetin was able to promote Lactobacillus in the cecum, which enhanced the gastrointestinal tract health. In summary, these results indicated that quercetin ameliorated the oxidized oil–induced oxidative stress by upregulating the transcription of Nrf2 and its downstream genes to restore redox balance and reinforced the intestinal barrier via higher expression and secretion of MUC2 and facilitating the growth of Lactobacillus in the cecum. Therefore, quercetin could be a potential feed additive that can be applied in poultry production for amelioration of oxidative stress caused by oxidized oil and preventing the potential invasion of exogenous pathogens.

The gastrointestinal tract is exposed to pro-oxidants from food, host immune factors, and microbial pathogens, which may induce oxidative damage. Oxidative stress has been shown to play an important role in the onset of inflammatory bowel disease. This study aimed to use a novel model to evaluate the effects of a screened natural component and explore its possible mechanism. An in vitro oxidative stress Caco2 cell model induced by H 2 O 2 was established using a realtime cellular analysis system and verified by addition of glutathione (GSH). A variety of plant components were chosen for the screening. Quercetin was the most effective phytochemical to alleviate the decreased cell index caused by H 2 O 2 among the tested plant components. Furthermore, quercetin ameliorated dextran sulfate sodium salt (DSS)-induced colitis and further increased the serum GSH. The mechanism of quercetin protection was explored in Caco2. Reversed H 2 O 2 -induced cell damage and decreased reactive oxygen species and apoptosis ratio were observed in quercetintreated cells. Also, quercetin increased expression of the glutamate-cysteine ligase catalytic subunit (GCLC), the first rate-limiting enzyme of glutathione synthesis, and increased intracellular GSH concentration under H 2 O 2 treatment. This effect was abolished by the GCLC inhibitor buthionine sulfoximine. These results indicated that quercetin can improve cell proliferation and increase intracellular GSH concentrations by upregulating transcription of GCLC to eliminate excessive reactive oxygen species (ROS). Increased extracellular H 2 O 2 concentration induced by quercetin under oxidative stress was related to the inhibition of AQP3 and upregulation of NOX1/2, which may contribute to the observed protective effects of quercetin. Moreover, the novel H 2 O 2 -induced oxidative stress cell model based on the real-time cellular analysis system was an effective model to screen natural products to deal with intestinal oxidative damage and help accelerate the discovery of new drugs for inflammatory bowel disease (IBD).

Salmonella Typhimurium ( S. Typhimurium) infection in broiler chickens threatens public health and livestock production. In this study, we explored the effects of highly nutritious (crude protein 21.8%, metabolizable energy 3.16 Mcal/kg) and lowly nutritious (crude protein 18.1%, metabolizable energy 2.98 Mcal/kg) diets on S. Typhimurium infection by altering the intestinal morphology and environment in broiler chickens. The highly nutritious diet significantly increased the body weight gain and reduced feed conversion ratio on day 1 to 21 ( P < 0.01). The highly nutritious diets promoted the intestinal villus height, crypt depth, and their ratio to improve the intestinal epithelial maturation ( P < 0.05). Highly nutritious diets significantly increased the expression of claudin-1, occludin, and NF-κB genes in the intestinal epithelium on the days of 14 and 21 ( P < 0.05). S. Typhimurium activated the expression of TLR4 , MyD88 , and NF-κB genes to cause an inflammatory response. The S. Typhimurium can increase the activity of myeloperoxidase, which cause an inflammatory response. The S. Typhimurium significantly reduced the diversity indexes of the ileal microbiota ( P < 0.05), increased the abundance of Cyanobacteria which can synthesize toxins. The highly nutritious diet group challenged with S. Typhimurium can increase the abundance of Lactobacillus in the ileum, which lead to improved intestinal health ( P < 0.05). It is concluded that increasing the nutritional level of dietary is beneficial to improve the resistance to S. Typhimurium infection by altering the intestinal bacterial community.