The current study was carried out to examine the effects of pueraria extract (PE) and curcumin (CUR) on growth performance, antioxidant capacity and intestinal integrity in broiler chickens. A complete randomized design with a 2 × 2 factorial arrangement of treatments was employed to assign 200 one-day-old Ross-308 broilers to four groups, each including five replicates of ten birds. Chickens in the control group (CON) were fed the basal diet, while the PE, CUR and PE+CUR groups were supplemented with 200 mg/kg PE or 200 mg/kg CUR or 200 mg/kg PE+ 200 mg/kg CUR. This trial lasted for 28 days. The PE supplementation decreased the average daily gain during the whole period (p < 0.05). The PE+CUR group had a higher feed conversion ratio than that of the PE and CUR groups during days 14–28 and 1–28 (p < 0.05). Dietary CUR supplementation increased duodenal T-SOD activity (p < 0.05). Compared with the CON group, the other three groups increased the duodenal GSH-Px activity, the PE+CUR group reduced the duodenal H₂O₂ level, and the CUR and PE groups elevated the ileal GSH-Px activity and the ratio of jejunal villus height to crypt depth, respectively (p < 0.05). The addition of PE decreased crypt depth and increased villus area and mucin-2 mRNA level in the jejunum (p < 0.05). Overall, dietary supplementation with PE, CUR, or a combination of these, enhanced the antioxidant status and intestinal integrity of broilers.

Porcine epidemic diarrhea virus (PEDV) has developed as a global problem for the pig business, resulting in significant financial losses. Black soldier fly extract (BFE) has been proven to improve intestinal growth in pigs after weaning. Consequently, the goal of the present investigation was to explore the effects of BFE supplementation on intestinal function in PEDV-infected piglets. Eighteen piglets were randomly allocated to three groups: control, PEDV, and BFE + PEDV. The piglets in the BFE + PEDV group received 500 mg/kg BW of BFE orally for seven days from day 4 to 10 of the study. On day 9 of the study, six pigs from each group received either clean saline or PEDV solution at a dosage of 10⁶ TCID₅₀ (50% tissue culture infectious dose) per pig. On day 11, samples of blood and intestine were taken for additional investigation. The results indicated a significant decrease in the average daily gain (ADG) of piglets infected with PEDV (p < 0.05). Additionally, PEDV infection led to an alteration of blood indexes and a reduction in plasma D-xylose concentration and villi height in the small intestine, while it increased plasma diamine oxidase activity and small intestinal crypt depth in piglets (p < 0.05). The PEDV infection significantly reduced antioxidant enzyme activity in plasma and the gut, including total superoxide dismutase and catalase, while increasing contents of oxidation-relevant products such as malondialdehyde and hydrogen peroxide in piglets. Moreover, PEDV infection increased the mRNA expression level of antiviral-related genes (p < 0.05). Nutritional supplementation with BFE improved intestinal histomorphological indicators and reduced oxidative stress produced by PEDV infection in piglets. Interestingly, BFE could significantly promote the mRNA expression level of antiviral-related genes in the ileum (p < 0.05). Overall, the preliminary results suggest that dietary BFE could improve intestinal function in piglets after PEDV infection. Currently, the findings put a spotlight on the role of BFE in the prevention and treatment of PED in piglets.

The impact of ZnO as a feed additive on growth-performance and intestinal function of Enterotoxigenic Escherichia coli (ETEC) K88-infected piglets remains unclear. Fecal scores of piglets in ETEC group were significantly increased compared to control group. ETEC K88 significantly damages the small intestine, including a reduction in villus height in the jejunum, duodenum, and ileum, and a decrease in total superoxide dismutase activity in the jejunum and catalase activity in the ileum and jejunum. Compared to control group, ETEC K88 infection significantly elevated the mRNA level of gene IL-1β and the level of ileal epithelial cell apoptosis. ZnO administration significantly alleviated these negative effects and improved the antioxidative capability of the ileum. Moreover, ZnO supplementation alleviated the imbalance of gut microbiota by restoring the reduced amount of Enterococcus and Lactobacillus in the jejunum, Clostridium in the ileum, and Lactobacillus in the cecum, as well as the increased amount of total eubacteria in the ileum and Enterococcus in the cecum induced by the ETEC K88 infection. In conclusion, ZnO administration can reduce the diarrhea of piglets infected with ETEC K88 by reducing the structural damage of the intestine, attenuating intestinal oxidative stress and epithelial cell apoptosis, and modulating the gut microbiota.

This study aimed to assess whether dietary supplementation with probiotics could alleviate intestinal injury in lipopolysaccharide (LPS)-challenged piglets. Healthy weaned piglets were randomly allocated to four individual groups (n = 6): (1) a control group; (2) an LPS group; (3) an LPS + Lactobacillus group; and (4) an LPS + Bacillus group. The control and LPS groups received a basal diet, while the probiotic groups were provided with the same basal diet supplemented with 6 × 10⁶ cfu/g of Lactobacillus casei (L. casei) or a combination of Bacillus subtilis (B. subtilis) and Bacillus licheniformis (B. licheniformis) at a dosage of 3 × 10⁶ cfu/g, respectively. On day 31 of the trial, overnight-fasted piglets were killed following the administration of either LPS or 0.9% NaCl solution. Blood samples and intestinal tissues were obtained for further analysis several hours later. The results indicate that dietary supplementation with probiotics significantly exhibited health-promoting effects compared with the control group and effectively reduced LPS-induced histomorphological damage to the small intestine, impairments in barrier function, and dysregulated immune responses via modulation of enzyme activity and the expression of relevant genes, such as nuclear factor-kappa B (NF-κB), interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 10 (IL-10), claudin-1, nuclear-associatedantigenki-67 (Ki-67), and β-defensins-1 (pBD-1). Collectively, these results suggest that dietary supplementation with probiotics could alleviate LPS-induced intestinal injury by enhancing the immunity and anti-inflammatory responses in piglets. Our research provides a theoretical basis for the rational application of probiotics in the future.

Porcine epidemic diarrhea virus (PEDV) causes severe intestinal damage, posing significant threats to the swine industry. Fucoidan (FUC), a biologically active compound, exhibits antiviral activity against multiple viruses. This study aimed to investigate the protective effects of FUC on PEDV-induced intestinal injury in piglets and explore its underlying mechanisms. A total of 28 healthy crossbred piglets were randomly allocated into four experimental groups using a 2 × 2 factorial design: (1) a control group, (2) an FUC group, (3) a PEDV group, and (4) an FUC+PEDV group. From day 4 to day 10, the piglets in the FUC and FUC+PEDV groups were orally administered fucoidan at a dosage of 20 mg/kg body weight (BW) each day. On day 8, the piglets in the PEDV and FUC+PEDV groups were orally administered PEDV at a dose of 3 × 10^5.5 TCID₅₀. The results show that FUC supplementation significantly decreased plasma DAO activity (p < 0.05) and increased the villus height, villus area, as well as the villus height/crypt depth (p < 0.05) in the intestine when compared to the PEDV-infected piglets. This indicates that FUC could alleviate the disruption of intestinal morphology and function caused by PEDV infection. FUC enhanced the antioxidant capacity of the piglets by increasing SOD and GSH-Px activity. Transcriptional profiling combined with quantitative analysis revealed that FUC regulates immune responses, substance transport, and arginine metabolism. Notably, FUC downregulated arginase 1 expression, which may redirect arginine toward nitric oxide synthesis, thereby establishing an antiviral state in the host. These findings highlight the potential application of FUC as a natural agent for mitigating PEDV-induced intestinal damage and improving gut health. Additionally, monitoring the health status of piglets is necessary when FUC is applied in practical applications.

Porcine epidemic diarrhea virus (PEDV) imposes substantial economic losses on the global swine industry owing to its high pathogenicity and transmissibility. Although arginine (Arg) is known to support the integrity of intestinal barrier, it is not clear whether Arg can alleviate intestinal injury induced by PEDV. A total of 32 healthy 7-day-old piglets were randomly assigned to four groups (Control, Arg, PEDV, PEDV + Arg; eight replicates per group). From day 5, piglets in the Arg and PEDV + Arg groups were orally administered Arg at 400 mg/kg body weight until day 11; then, PEDV (1 × 10^5.5 TCID₅₀) was given orally for two PEDV-infected groups. On day 14, all piglets were slaughtered to obtain blood and intestine samples for further analysis. The results showed that PEDV infection significantly reduced T-SOD and CAT activities in plasma and intestine while elevating MPO levels. Arg supplementation restored T-SOD (plasma, duodenum, ileum), CAT (plasma, ileum), and GSH-Px (jejunum, ileum) activities and reduced MDA (jejunum) content in PEDV-infected piglets. Hematological analysis showed Arg alleviated PEDV-induced increases in MCV and RDW-SD, and significantly elevated MCHC. The real-time quantitative PCR analysis demonstrated that Arg further enhanced PEDV structural genes (M, N, S) expression in the duodenum, ileum, and colon. Concurrently, Arg significantly up-regulated interferon-stimulated genes (MX1, OASL, ISG15, IFITM3) in the ileum, IRF7 in the duodenum and colon, and IFN-β in the ileum. Arg also down-regulated the pro-inflammatory cytokines IL-6 and CXCL2 and the antimicrobial peptide REG3G in the colon, while up-regulating the tissue repair gene MMP13 in the ileum. In conclusion, oral Arg exhibits a unique dual role: it promotes PEDV replication to a certain extent while significantly enhancing antioxidant capacity, strengthening intestinal antiviral immunity, and attenuating intestinal inflammation. These findings highlight Arg’s role in promoting disease tolerance and offer a novel perspective for nutritional intervention strategies against PEDV infection.