Ficus pandurata Hance Inhibits Ulcerative Colitis and Colitis-Associated Secondary Liver Damage of Mice by Enhancing Antioxidation Activity

Inflammatory bowel disease (IBD), a global disease threatening human health, is commonly accompanied by secondary liver damage (SLD) mediated by the gut-liver axis. Oxidative stress acts a critical role in the onset of IBD, during which excessive oxidation would destroy the tight junctions between intestinal cells, promote proinflammatory factors to penetrate, and thereby damage the intestinal mucosa. Ficus pandurata Hance (FPH) is widely used for daily health care in South China. Our previous study showed that FPH protected acute liver damage induced by alcohol. However, there is no study reporting FPH treating ulcerative colitis (UC). This study is designed to investigate whether FPH could inhibit UC and reveal its potential mechanism. The results showed that FPH significantly alleviated the UC disease symptoms including the body weight loss, disease activity index (DAI), stool consistency changing, rectal bleeding, and colon length loss of UC mice induced by dextran sulfate sodium (DSS) and reversed the influences of DSS on myeloperoxidase (MPO) and diamine oxidase activity (DAO). FPH suppressed UC via inhibiting the TLR4/MyD88/NF-κB pathway and strengthened the gut barrier of mice via increasing the expressions of ZO-1 and occludin and enhancing the colonic antioxidative stress property by increasing the levels of T-SOD and GSH-Px and the expressions of NRF2, HO-1, and NQO1 and reducing MDA level and Keap1, p22-phox, and NOX2 expressions. Furthermore, FPH significantly inhibited SLD related to colitis by reducing the abnormal levels of the liver index, ALT, AST, and cytokines including TNFα, LPS, LBP, sCD14, and IL-18 in the livers, as well as decreasing the protein expressions of NLRP3, TNFα, LBP, CD14, TLR4, MyD88, NF-κB, and p-NF-κB, suggesting that FPH alleviated UC-related SLD via suppressing inflammation mediated by inhibiting the TLR4/MyD88/NF-κB pathway. Our study firstly investigates the anticolitis pharmacological efficacy of FPH, suggesting that it can be enlarged to treat colitis and colitis-associated liver diseases in humans.

Dietary corn resistant starch regulates intestinal morphology and barrier functions by activating the Notch signaling pathway of broilers

Objective: This study was conducted to investigate the effects of dietary corn resistant starch (RS) on the intestinal morphology and barrier functions of broilers.Methods: A total of 320 one-day-old broilers were randomly allocated to 5 dietary treatments: one normal corn–soybean (NC) diet, one corn–soybean–based diet supplementation with 20% corn starch (CS), and 3 corn–soybean–based diets supplementation with 4%, 8%, and 12% corn resistant starch (RS) (identified as 4% RS, 8% RS, and 12% RS, respectively). Each group had eight replicates with eight broilers per replicate. After 21 days feeding, one bird with a body weight (BW) close to the average BW of their replicate was selected and slaughtered. The samples of duodenum, jejunum, ileum, caecum digesta, and blood were collected.Results: Birds fed 4% RS, 8% RS and 12% RS diets showed lower feed intake, BW gain, jejunal villus height (VH), duodenal crypt depth (CD), jejunal VH/CD ratio, duodenal goblet cell density as well as mucin1 mRNA expressions compared to the NC group, but showed higher concentrations of cecal acetic acid and butyric acid, percentage of jejunal proliferating cell nuclear antigen-positive cells and delta like canonical Notch ligand 4 (Dll4), and hes family bHLH transcription factor 1 mRNA expressions. However, there were no differences on the plasma diamine oxidase activity and D-lactic acid concentration among all groups.Conclusion: These findings suggested that RS could suppress intestinal morphology and barrier functions by activating Notch pathway and inhibiting the development of goblet cells, resulting in decreased mucins and tight junction mRNA expression.

Abscisic Acid Promotes γ-Aminobutyric Acid Accumulation in Soybean Germinating Under Hypoxia-NaCl Stress

γ-aminobutyric acid is a nonprotein amino acid that accumulates in plants under stress. Abscisic acid is important for stress regulation via modulation of γ-aminobutyric acid function. Our results show that the expression of glutamate decarboxylase but not diamine oxidase gene is upregulated in germinating soybean treating treated with exogenous abscisic acid. There was a concomitant increase in glutamate decarboxylase and diamine oxidase activities and putrescine and spermine contents with a decrease in glutamate. These changes were abrogated by fluridone, an inhibitor of abscisic acid synthesis. In conclusion, abscisic acid treatment increases γ-aminobutyric acid accumulation by upregulating diamine oxidase gene expression and activation of glutamate decarboxylase and diamine oxidase activity in germinating soybean under hypoxia-salt stress.

Influence of Mushroom Polysaccharide, Nano-Copper, Copper Loaded Chitosan, and Lysozyme on Intestinal Barrier and Immunity of LPS-mediated Yellow-Feathered Chickens

This study investigated the influence of dietary supplementation with some antibiotic alternatives on growth performance, intestinal barrier, and immunity of lipopolysaccharide (LPS) challenged chicks. Wenshi females, aged 4 days, were allocated randomly into eight groups, each with six replicates of 20 birds (n = 120/treatment), which received a basal diet supplemented with 0 (control), 0 (LPS), 200 mg/kg aureomycin, 50 mg/kg mushroom polysaccharide, 100 mg/kg mushroom polysaccharide, 500 mg/kg nano-copper, 300 mg/kg copper loaded chitosan, and 500 mg/kg lysozyme for 21 days. On day 18 and 20, the control birds were injected with 0.5 mL saline solution, the other treatments were injected with 0.5 mL saline containing 500 µg LPS/kg body weight (BW). The results indicated that LPS treatment reduced the BW, average daily gain (ADG), and daily feed intake (ADFI) than the controls (p < 0.05), and the antibiotic and the tested alternatives could not retrieve the normal BW, ADG, and ADFI. The tested additives reduced several negative effects of LPS; they reduced diamine oxidase activity and inflammatory mediators in plasma, jejunal mucosa, spleen and thymus, increased content of immunoglobulin in plasma and jejunal mucosa, and decreased gene expression of inducible nitric oxide synthase and Cyclooxygenase 2 in jejunal mucosa.