The present study was performed to evaluate the antioxidant and intestinal protective effects of baicalin-copper on deoxynivalenol-challenged piglets. Forty weaned piglets were randomly divided into four groups and assigned to different diets: (1) basal diet (Con), (2) 4 mg/kg deoxynivalenol of basal diet (DON), (3) 5 g/kg baicalin-copper of basal diet (BCU); and (4) 4 mg/kg deoxynivalenol+5 g/kg baicalin‐copper of basal diet (DBCU). The results showed that the ADFI and ADG of piglets in the DON group were markedly lower than those in the Con group, but the ADFI and ADG of the DBCU group were not significantly different from those of the Con group. In piglets fed a DON-contaminated diet, dietary supplementation with BCU significantly decreased the mRNA levels of P70S6K, 4E-BP1, and HSP70 in the liver, the protein expression of HO-1 in the jejunum, and the expression of p-Nrf2 and p-NF-κB in the ileum but increased Mn-SOD activity in serum. Dietary supplementation with BCU increased jejunal maltase, ZIP4 and MT mRNA levels, and serum concentrations of Arg, Val, Ile, Leu, Lys, and Tyr in DON-contaminated piglets. In summary, BCU can alleviate the growth impairment induced by DON and enhance antioxidant capacity and nutrition absorption in piglets fed DON-contaminated diets.

Medium-chain fatty acid glycerides have been shown to provide energy for rapid oxidation in the body. The study was conducted to investigate the effects of dietary supplementation with medium-chain fatty acid glyceride on the growth performance and intestinal health of weaned piglets fed with a low-protein diet. Nighty healthy weaned piglets were randomly divided into five treatments: NP (Normal protein treatment, normal-protein diet no antibiotics included); NC (Negative control, low-protein diet no antibiotics included); PC (Positive control, low-protein diet +75 mg/kg quinocetone, 20 mg/kg virginiamycin and 50 mg/kg aureomycin); MCT (tricaprylin + tricaprin treatment, low-protein diet + tricaprylin + tricaprin); GML (glycerol monolaurate treatment, low-protein diet + glycerol monolaurate). The results showed that the average daily feed intake (ADFI) of the MCT treatment was significantly higher than that of the NP, NC treatments (p < 0.05). In the jejunum, the villus height of the GML treatment was significantly lower than that of the PC treatment (p < 0.05), and the number of goblet cells in the GML treatment was higher than that in the NC treatment (p < 0.05). Compared with the NC treatment, the MCT treatment significantly increased the level of claudin-1, Zonula occludens-1(ZO-1), while the GML treatment significantly increased the level of claudin-1, occludin, ZO-1 (p < 0.05). In the ileum, the level of ZO-1 in the GML treatment was significantly higher than that in the NP, NC, PC treatments (p < 0.05). Compared with the NC treatment, the GML treatment significantly increased the level of Secretory immunoglobulin A (SIgA) in the ileum and serum, while the MCT treatment significantly increased the level of SIgA and decreased the level of interleukin-6 (IL-6) in the ileum (p < 0.05). These results showed that the addition of medium-chain fatty acid glycerides to a low-protein diet could improve the growth performance and intestinal functional barrier of weaned piglets and also improve the immune function of weaned piglets.

Background: Deoxynivalenol contamination is increasing worldwide, presenting great challenges to food security and causing great economic losses in the livestock industry. Objective: This study was conducted to determine the protective effect of baicalin zinc as a dietary supplement on pigs fed with a deoxynivalenol-contaminated diet. Method: A total of 40 weaned pigs (21 d of age; 6.13 ± 0.42 kg average BW) were randomly assigned (10 pigs/group) to 4 dietary treatments: basal diet (Con group), basal diet + 4 mg/kg DON (DON group), basal diet + 5 g/kg BZN (BZN group), and basal diet + 5 g/kg BZN + 4 mg/kg DON (DBZN group) for a 14-d period. Seven randomly selected pigs from each treatment were killed for blood and tissue sampling. Results: The results showed that piglets challenged with DON exhibited significantly reduced levels of ADG, ADFI, and F/G (p <0.05). BZN supplemented diets significantly suppressed the protein expression of p-Nrf2, p-NF-kB, and HO-1 in the intestine of DON challenged piglets (p < 0.05). In liver, DON markedly increased the mRNA expression of P70S6K and HSP70 in piglets fed the basal diet, but significantly reduced that of HO-1, NQO-1, NF-kB, AMPKα2 and HSP70 in piglets fed the BZN supplemented diet (p < 0.05). Dietary supplementation with BZN markedly increased the T-AOC level of serum in weaned piglets (p < 0.05). In jejunum, dietary supplementation with BZN activated the mRNA expression of ZIP4 in piglets (p < 0.05), BZN supplementation significantly suppressed the activity of sucrose and increased the protein concentration in chyme (p < 0.05). Conclusion: BZN can play a protective role by reducing oxidative stress and enhancing nutrition absorption in pigs fed DON-contaminated diets.

Background Gut health plays a vital role in the overall health and disease control of human and animals. Intestinal oxidative stress is a critical player in the induction and progression of cachexia which is conventionally diagnosed and classified by weight loss. Therefore, reduction of intestinal oxidative injury is a common and highly effective strategy for the maintenance of human and animal health. Here we identify intestinal myeloid differentiation primary response gene 88 (MyD88) as a novel target for intestinal oxidative stress using canonical oxidative stress model induced by paraquat (PQ) in vitro and in vivo. Methods Intestinal oxidative stress was induced by administration of PQ in intestinal epithelial cells (IECs) and mouse model. Cell proliferation, apoptosis, DNA damage, mitochondrial function, oxidative status, and autophagy process were measured in wild-type and MyD88-deficient IECs during PQ exposure. Autophagy inhibitor (3-methyladenine) and activator (rapamycin) were employed to assess the role of autophagy in MyD88-deficient IECs during PQ exposure. MyD88 specific inhibitor, ST2825, was used to verify function of MyD88 during PQ exposure in mouse model. ResultsMyD88 protein levels and apoptotic rate of IECs are increased in response to PQ exposure (P < 0.001). Intestinal deletion of MyD88 blocks PQ-induced apoptosis (~42% reduction) and DNA damage (~86% reduction), and improves mitochondrial fission (~37% reduction) and function including mitochondrial membrane potential (~23% increment) and respiratory metabolism capacity (~26% increment) (P < 0.01). Notably, there is a marked decrease in reactive oxygen species in MyD88-deficient IECs during PQ exposure (~70% reduction), which are consistent with high activity of antioxidative enzymes (~83% increment) (P < 0.001). Intestinal ablation of MyD88 inhibits mTOR signalling, and further phosphorylates p53 proteins during PQ exposure, which eventually promotes intestinal autophagy (~74% increment) (P < 0.01). Activation of autophagy (rapamycin) promotes IECs growth as compared with 3-methyladenine-treatment during PQ exposure (~173% increment), while inhibition of autophagy (3methyladenine) exacerbates oxidative stress in MyD88-deficient IECs (P < 0.001). In mouse model, inhibition of MyD88 using specific inhibitor ST2825 followed by PQ treatment effectively ameliorates weight loss (~4% increment), decreased food intake (~92% increment), gastrocnemius and soleus loss (~24% and ~20% increment, respectively), and intestinal oxidative stress in an autophagy dependent manner (P < 0.01). Conclusions MyD88 modulates intestinal oxidative stress in an autophagy-dependent mechanism, which suggests that reducing MyD88 level may constitute a putative therapeutic target for intestinal oxidative injury-induced weight loss.

The present experiment assessed the inflammatory responses, hormone secretion, and gut microbiota of weanling piglets administered baicalin-copper complex (BCU) or deoxynivalenol (DON) supplementation diets. Twenty-eight piglets were randomly assigned to four groups: control diet (Con group), a 4 mg DON/kg diet (DON group), a 5 g BCU/kg diet (BCU group), a 5 g BCU + 4 mg DON/kg diet (DBCU group). After 14 days, the results showed that dietary BCU supplementation remarkably increased the relative abundance of Clostrium bornimense and decreased the relative abundance of Lactobacillus in the DBCU group (p < 0.05). BCU decreased the serum concentration of IgG, IL-2, IFN-γ, and IgA in DON treated piglets (p < 0.05), and promoted the serum concentration of IL-1β, IgG, IL-2, IFN-γ, IgA, IL-6, IgM, and TNFα in normal piglets (p < 0.05). BCU increased the concentrations of serum IGF1, insulin, NPY, GLP-1, and GH, and decreased the concentrations of serum somatostatin in no DON treated piglets (p < 0.05). Dietary BCU supplementation significantly promoted the secretion of somatostatin, and inhibited the secretion of leptin in piglets challenged with DON (p < 0.05). BCU regulated the expression of food intake-related genes in the hypothalamus and pituitary of piglets. Collectively, dietary BCU supplementation alleviated inflammatory responses and regulated the secretion of appetite-regulating hormones and growth-axis hormones in DON challenged piglets, which was closely linked to changes of intestinal microbes.

We investigated the effects of rapamycin (RAPA) and chloroquine (CQ) in supporting growth performance and the intestinal mucosal barrier in response to deoxynivalenol (DON) in piglets. A total of 32 healthy weaned piglets (bodyweight 7.10±0.58 kg) were divided into four groups and treated daily with RAPA (1 mg/kg BW), CQ (10 mg/kg BW), or a control volume of normal saline (two groups) until the end of the experiment. After feeding a basal diet for seven days, three groups were then switched to mildewed feed containing 1 mg kg/DON for a further seven days. In contrast to the control group, DON-treated piglets showed decreased average daily gain (ADG) and daily feed intake (ADFI), as well as negatively affected intestinal morphology as indicated by villus height, crypt depth, and tight junction protein expression. A group treated with RAPA and DON showed increased intestinal autophagy, aggravated inflammatory responses, and damage to the intestinal mucosa and permeability, leading to reduced growth performance. Meanwhile, a group treated with CQ and DON showed indices comparable to the non-DON control group, with alleviated inflammatory cytokines and healthy intestinal morphology and structure. They also showed better growth performance compared to DON treatment alone. These findings have important implications for mediating autophagy against DON in vivo, as well as the potential for CQ in improving growth performance and maintaining intestinal barrier integrity in weanling piglets.

Individuals with postnatal growth retardation (PGR) are prone to developing chronic diseases. Abnormal development in small intestine is casually implicated in impaired growth. However, the exact mechanism is still implausible. In this present study, PGR piglets (aged 42 days) were employed as a good model to analyze developmental changes in intestinal mucosal barrier function. Our data demonstrated that PGR piglets exhibited impaired jejunal and ileal epithelial villous morphology and permeability, accompanied by decreased cell proliferation ability and increased apoptosis rate. In addition, the expression of tight junction proteins (ZO‐1, claudin 1, and occludin) and E‐cadherin was markedly inhibited by PGR. The expression of P‐glycoprotein was significantly reduced in PGR piglets, as well as decreased activity of lysozyme. Moreover, the mRNA abundance and content of inflammatory cytokines were significantly increased in the intestinal mucosa and plasma of PGR piglets, respectively. PGR also contributed to lower level of sIgA, and higher level of CD68‐positive rate, β‐defensins, and protein expression involved p38 MAPK/NF‐κB pathway. Furthermore, PGR altered the intestinal microbial community such as decreased genus Alloprevotella and Oscillospira abundances, and led to lower microbial‐derived butyrate production, which may be potential targets for treatment. Collectively, our findings indicated that the intestinal mucosal barrier function of PGR piglets could develop the nutritional intervention strategies in prevention and treatment of the intestinal mucosal barrier dysfunction in piglets and humans.

This study aimed to investigate the beneficial effect of baicalin–zinc complex (BZN) on intestinal microorganisms in deoxynivalenol (DON)-challenged piglets and the association between intestinal microorganisms and host immunity and hormone secretion. Forty weaned piglets were randomly divided into four treatments with 10 piglets in each treatment: (1) control (Con) group (pigs fed basal diet); (2) DON group (pigs fed 4 mg DON/kg basal diet); (3) BZN group (pigs fed 0.5% BZN basal diet); and (4) DBZN group (pigs fed 4 mg DON/kg and 0.5% BZN basal diet). The experiment lasted for 14 days. The BZN supplementation in DON-contaminated diets changed the intestinal microbiota composition and increased intestinal microbial richness and diversity of piglets. The BZN supplementation in DON-contaminated diets also alleviated the inflammatory responses of piglets and modulated the secretion of hormones related to the growth axis. Moreover, microbiota composition was associated with inflammatory and hormone secretion. In conclusion, BZN alleviated inflammatory response and hormone secretion in piglets, which is associated with the intestinal microbiome.