Suboptimal embryonic/fetal survival and growth remains a significant problem in mammals. Using a swine model, we tested the hypothesis that dietary L-arginine supplementation during gestation may improve pregnancy outcomes through enhancing placental growth and modulating hormonal secretions. Gestating pigs (Yorkshire×Landrace, n=108) were assigned randomly into two groups based on parity and body weight, representing dietary supplementation with 1.0% L-arginine-HCl or 1.7% L-alanine (isonitrogenous control) between days 22 and 114 of gestation. Blood samples were obtained from the ear vein on days 22, 40, 70 and 90 of gestation. On days 40, 70 and 90 of gestation, concentrations of estradiol in plasma were higher (P<0.05) in arginine-supplemented than in control sows. Moreover, arginine supplementation increased (P<0.05) the concentrations of arginine, proline and ornithine in plasma, but concentrations of urea or progesterone in plasma did not differ between the two groups of sows. Compared with the control, arginine supplementation increased (P<0.05) the total number of piglets by 1.31 per litter, the number of live-born piglets by 1.10 per litter, the litter birth weight for all piglets by 1.36 kg, and the litter birth weight for live-born piglets by 1.70 kg. Furthermore, arginine supplementation enhanced (P<0.05) placental weight by 16.2%. The weaning-to-estrus interval of sows was not affected by arginine supplementation during gestation. These results indicate that dietary arginine supplementation beneficially enhances placental growth and the reproductive performance of sows.
The objective of this study was to investigate the effects of Lactobacillus reuteri LR1, a new strain isolated from the feces of weaned pigs, on the growth performance, intestinal morphology, immune responses, and intestinal barrier function in weaned pigs. A total of 144 weaned pigs (Duroc × Landrace × Yorkshire, 21 d of age) with an initial BW of 6.49 ± 0.02 kg were randomly assigned to 3 dietary treatments with 8 replicate pens, each of per treatment and 6 pigs. Pigs were fed a basal diet (CON, controls), the basal diet supplemented with 100 mg/kg olaquindox and 75 mg/kg aureomycin (OA) or the basal diet supplemented with 5 × 1010 cfu/kg L. reuteri LR1 for a 14-d period. At the end of study, the ADG, ADFI, and G:F were calculated, and 1 randomly selected pig from each pen was euthanized for sample collection. The LR1 increased ADG (22.73%, P < 0.05) compared with CON. The villus height of the ileum was increased (P < 0.05) and crypt depth in duodenum was reduced (P < 0.05), along with increased (P < 0.05) villus height to crypt depth ratio of the jejunum and ileum by LR1 compared with CON and OA. LR1 increased (P < 0.05) ileal mucosal content of IL-22 and transforming growth factor-β compared with OA. Compared with CON, LR1 increased (P < 0.05) and OA decreased (P < 0.05) the ileal content of secretory immunoglobulin A (sIgA), and the abundance of transcripts of porcine β-defensin 2 and protegrin 1-5. Compared with CON, LR1 increased (P < 0.05) tight junction protein zonula occludens-1 and occludin transcripts in the mucosa of the jejunum and ileum, and those of mucin-2 in ileal mucosa. The relative expression of toll-like receptor 2 (TLR2) and TLR4 were increased (P < 0.05) in ileal mucosa in pigs fed LR1 compared with CON. In conclusion, these data indicated that dietary LR1 supplementation at 5 × 1010 cfu/kg improved growth performance, intestinal morphology, and intestinal barrier function in weaned pigs.
Background Deoxynivalenol (DON) is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals. Resveratrol (RES) effectively exerts anti-inflammatory and antioxidant effects. However, the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear. Therefore, this study aimed to investigate the effect of RES on growth performance, gut health and the gut microbiota in DON-challenged piglets. A total of 64 weaned piglets [Duroc × (Landrace × Yorkshire), 21-d-old, 6.97 ± 0.10 kg body weight (BW)] were randomly allocated to 4 treatment groups (8 replicate pens per treatment, each pen containing 2 males; n = 16 per treatment) for 28 d. The piglets were fed a control diet (CON) or the CON diet supplemented with 300 mg RES/kg diet (RES group), 3.8 mg DON/kg diet (DON) or both (DON+RES) in a 2 × 2 factorial design. Results DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) mRNA and protein expression, and increased zonula occludens-1 (ZO-1) mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet (P < 0.05). Compared with unsupplemented DON-challenged piglets, infected piglets fed a diet with RES showed significantly decreased malondialdehyde (MDA) levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes (i.e., GCLC, GCLM, HO-1, SOD1 and NQO-1) and glutamate-cysteine-ligase modulatory subunit (GCLM) protein expression (P < 0.05). Moreover, RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets (P < 0.05). Finally, RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations, while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone (P < 0.05). Conclusions RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function, alleviating intestinal inflammation and oxidative damage, and positively modulating the gut microbiota. The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations, and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.
This study aimed to explore the effect of L-arginine on lipopolysaccharide (LPS)-induced inflammatory response and oxidative stress in IPEC-2 cells. We found that the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), cluster of differentiation 14 (CD14), nuclear factor-kappaBp65 (NF-κBp65), chemokine-8 (IL-8), tumor necrosis factor (TNF-α) and chemokine-6 (IL-6) mRNA were significantly increased by LPS. Exposure to LPS induced oxidative stress as reactive oxygen species (ROS) and malonaldehyde (MDA) production were increased while glutathione peroxidase (GSH-Px) were decreased in LPS-treated cells compared to those in the control. LPS administration also effectively induced cell growth inhibition through induction of G0/G1 cell cycle arrest. However, compared with the LPS group, cells co-treatment with L-arginine effectively increased cell viability and promoted the cell cycle into the S phase; L-arginine exhibited an anti-inflammatory effect in alleviating inflammation induced by LPS by reducing the abundance of TLR4, MyD88, CD14, NF-κBp65, and IL-8 transcripts. Cells treated with LPS+L-arginine significantly enhanced the content of GSH-Px, while they decreased the production of ROS and MDA compared with the LPS group. Furthermore, L-arginine increased the activity of arginase-1 (Arg-1), while Arg-1 inhibitor abolished the protection of arginine against LPS-induced inflammation and oxidative stress. Taken together, these results suggested that L-arginine exerted its anti-inflammatory and antioxidant effects to protect IPEC-J2 cells from inflammatory response and oxidative stress challenged by LPS at least partly via the Arg-1 signaling pathway.
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