The liver is an organ that produces large amounts of reactive oxygen species (ROS). Human infants or piglets are prone to oxidative damage due to their uncompleted development of the antioxidant system, causing liver disease. Piceatannol (PIC) has been found to have significant antioxidant effects. The aim of this experiment was to investigate the effects of PIC on the liver in piglets experiencing oxidative stress caused by diquat (DQ). After weaning, 54 male piglets (Duroc × [Landrace × Yorkshire]) were selected and randomly divided into three treatment groups: the CON group, the DQ-CON group, and the DQ-PIC group. The two challenged groups were injected with DQ and then orally administrated either PIC or another vehicle solution, while the control group was given sterile saline injections and an orally administrated vehicle solution. Compared to the results of the CON group, DQ increased the percentage of apoptosis cells in the liver, also decreased the amount of reduced glutathione (GSH) and increased the concentration of malondialdehyde (MDA). In addition, the adenosine triphosphate (ATP) production, activities of mitochondrial complex I, II, III, and V, and the protein expression level of sirtuin 1 (SIRT1) were inhibited by DQ. Furthermore, PIC supplementation inhibited the apoptosis of hepatic cells caused by DQ. PIC also decreased MDA levels and increased the amount of GSH. Piglets given PIC supplementation exhibited increased activities of mitochondrial complex I, II, III, and V, the protein expression level of SIRT1, and the ATP production in the liver. In conclusion, PIC affected the liver of piglets by improving redox status, preserving mitochondrial function, and preventing excessive apoptosis.

Background: The spleen is the primary reservoir of immune cells in mammals. Diverse stimuli can disrupt spleen homeostasis, resulting in spleen injury and immune dysfunction. This study employed a porcine model to assess the therapeutic potential of salvianolic acid B (SAB) against lipopolysaccharide (LPS)-induced splenic injury. Methods: Seventy-two male weanling piglets were randomly assigned to one of four groups: CON-SS, SAB-SS, CON-LPS, and SAB-LPS. The CON-SS and CON-LPS groups received a basal diet, while SAB-SS and SAB-LPS groups received a SAB-supplemented diet. After 14 d, the CON-SS and SAB-SS groups received an intraperitoneal injection of sterile saline, whereas the CON-LPS and SAB-LPS groups were injected with LPS. Blood and spleen tissues were harvested 6 h post-injection for biochemical analysis. Results: LPS induced systemic immune disorders in piglets, as evidenced by increased immune organ indices and decreased white blood cell, lymphocyte, and basophil counts in blood (p < 0.05). LPS also caused histoarchitectural disruption, cell apoptosis, oxidative stress, and inflammation in the spleen (p < 0.05). Conversely, SAB improved splenic histopathology and reduced splenic apoptosis and pro-inflammatory mediators in piglets (p < 0.05). SAB significantly mitigated peroxidation accumulation by facilitating the nuclear translocation of nuclear factor erythroid 2-related factor 2 and strengthening the antioxidant system, and inhibited nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome activation (p < 0.05). Mechanistically, SAB attenuated LPS-induced splenic oxidative stress and NLRP3 inflammasome activation by restoring mitochondrial structure and function (p < 0.05). Conclusions: This research unveils that SAB alleviates LPS-induced spleen disorder by reinforcing antioxidant system and suppressing NLRP3 inflammasome, highlighting SAB’s potential as a prospective therapeutic agent for spleen disorders.

The present study investigated the potential of polydatin to protect against liver injury and the mitochondrial dysfunction of weanling piglets suffering from intra-uterine growth retardation (IUGR). Thirty-six normal birth weight weanling piglets and an equal number of IUGR littermates were given a basal diet with or without polydatin (250 mg/kg) from 21 to 35 d of age. Plasma and liver samples were collected to measure biochemistry parameters at 35 d of age. IUGR caused hepatic apoptosis, mitochondrial dysfunction, and oxidative damage, along with a lower efficiency of energy metabolism and inferior antioxidant ability. Polydatin decreased apoptotic rate, improved the features of mitochondrial damage, inhibited mitochondrial swelling and superoxide anion formation, and preserved mitochondrial membrane potential in the liver. Concurrently, polydatin promoted mitochondrial biogenesis, increased sirtuin 1 activity, and upregulated the expression levels of several genes related to mitochondrial function and fitness. Polydatin also facilitated mitochondrial oxidative metabolism with a beneficial outcome of increased energy production. Furthermore, polydatin mitigated the IUGR-induced reduction in manganese superoxide dismutase activity and prevented the excessive accumulation of oxidative damaging products in the liver. These findings indicate that polydatin confers protection against hepatic injury and mitochondrial dysfunction in the IUGR piglets by improving energy metabolism and redox balance.

Background: Intestinal epithelial barrier dysfunction, a major consequence of inflammatory and oxidative stress, contributes to enteric disorder progression. Salvianolic acid B (SAB), a prominent water-soluble phenolic compound in Salvia miltiorrhiza, shows intestinal protective potential, but the underlying mechanisms remain unclear. Methods: This study investigated the protective effects of SAB on intestinal barrier function using a lipopolysaccharide (LPS)-challenged piglet model and LPS-stimulated IPEC-J2 cells. Results: SAB alleviated LPS-induced intestinal injury, evidenced by reduced plasma diamine oxidase and D-lactate levels, improved intestinal morphology, decreased pro-inflammatory cytokines, and enhanced antioxidant capacity. SAB also strengthened intestinal barrier integrity by increasing goblet cell number and mucin 2 levels and upregulating tight junction protein expression. Moreover, SAB restored epithelial proliferation–apoptosis balance and increased PI3K/AKT/mTOR phosphorylation. Molecular docking and molecular dynamics simulations predicted a stable SAB–PI3Kα/p110α interaction, whereas LY294002 treatment attenuated SAB-mediated restoration of epithelial renewal and barrier integrity in LPS-treated IPEC-J2 cells. SAB also altered the jejunal microbial composition, including higher relative abundance of Streptococcus and lower relative abundance of Escherichia-Shigella, together with increased jejunal acetate and lactate concentrations. Conclusions: SAB alleviates inflammation-associated intestinal barrier dysfunction by restoring epithelial proliferation–apoptosis balance and regulating the microbiota–metabolite profile.

A novel fungal phytase (NFP) was evaluated for its effects on growth performance, phosphorus (P) metabolism, tibia development, and nutrient digestibility in broilers. A total of 420 one-day-old Arbor Acres broilers were randomly assigned to seven treatments: a negative control (basal diet without phytase), a positive control (500 U/kg commercial phytase), and five groups supplemented with NFP at 250, 500, 1000, 1500, or 2000 U/kg. Increasing inclusion of dietary NFP linearly improved average daily gain and feed conversion ratio (FCR) during days 22–42 and overall, with NFP outperforming commercial phytase at equivalent doses in FCR reduction. NFP increased the digestibility of crude fiber and P, linearly increased crude protein digestibility, and dose-dependently enhanced ileal digestibility of several amino acids (especially at 1000–2000 U/kg). NFP dose-dependently increased plasma inorganic P while reducing alkaline phosphatase and parathyroid hormone. Tibia weight, midshaft width, bone density, breaking strength, and P content increased linearly with NFP, peaking at 1000–2000 U/kg. NFP also upregulated tibial mRNA expression of the phosphate-regulating gene with homology to endopeptidase on the X chromosome, dentin matrix protein 1, and osteocalcin. In conclusion, NFP optimizes broiler growth, nutrient utilization, and skeletal development via dose-dependent modulation of P metabolism and osteogenic pathways.