At present, the widespread use of high-dose zinc oxide and antibiotics to prevent post-weaning diarrhea (PWD) in piglets has caused serious environmental problems. To solve this problem, we studied the effect of HNa as a substitute for zinc oxide (ZnO) and antibiotics on the growth performance, immune status, and antioxidant capacity of piglets. Seventy-two weaned piglets (body weight = 7.42 ± 0.85 kg, 26-d-old) were distributed in a randomized 2 × 3 factorial design (two sexes and three treatments) with six replicates of four piglets each. The three treatments were the control diet (basic diet), HNa diet (basic diet + 2000 mg/kg sodium humate), and ZoA group (basic diet + 1600 mg/kg zinc oxide + 1000 mg/kg oxytetracycline calcium). ANOVA and Chi-square tests were applied to compare the means (p < 0.05) between treatments. The results showed that body weight at 16 and 30 d and the average daily gain of piglets fed with HNa or ZoA were significantly higher (p < 0.05) than the control group. Supplementing HNa or ZoA significantly increased (p < 0.05) the level of immunoglobulin M and G, and reduced (p < 0.05) the concentration of inflammatory factors such as tumor necrosis factor-alpha (TNF-α), interleukins IL-6 and IL-1β, myeloperoxidase (MPO), and diamine oxidase (DAO). Furthermore, dietary HNa or ZnO significantly reduced (p < 0.05) the level of total antioxidant capacity (T-AOC) and malondialdehyde (MDA) compared with the control group. ZoA treatment showed an upward trend of IgA level and a downward trend of the concentration of lipopolysaccharide (LPS) and catalase (CAT). Overall, the study demonstrated that the addition of HNa in the diet partially replaced antibiotics and ZnO to improve the growth performance, immune function, and antioxidant capacity of weaned piglets, and maintained a good preventive effect on piglet diarrhea.

Background: This study aimed to investigate whether the combination of Macleaya cordata extract (MCE) and Bacillus could improve the laying performance and health of laying hens better. Methods: A total of 360 29-week-old Jingbai laying hens were randomly divided into 4 treatments: control group (basal diet), MCE group (basal diet + MCE), Probiotics Bacillus Compound (PBC) group (basal diet + compound Bacillus), MCE + PBC group (basal diet + MCE + compound Bacillus). The feeding experiment lasted for 42 d. Results: The results showed that the laying rate and the average daily egg mass in the MCE + PBC group were significantly higher than those in the control group (P < 0.05) and better than the MCE and PBC group. Combination of MCE and Bacillus significantly increased the content of follicle-stimulating hormone (FSH) in the serum and up-regulated the expression of related hormone receptor gene (estrogen receptor-β, FSHR and luteinizing hormone/choriogonadotropin receptor) in the ovary of laying hens (P < 0.05). In the MCE + PBC group, the mRNA expressions of zonula occluden-1, Occludin and mucin-2 in jejunum was increased and the intestinal epithelial barrier detected by transmission electron microscopy was enhanced compared with the control group (P < 0.05). In addition, compared with the control group, combination of MCE and Bacillus significantly increased the total antioxidant capacity and catalase activity (P < 0.05), and down-regulated the mRNA expressions of inflammation-related genes (interleukin-1β and tumor necrosis factor-α) as well as apoptosis-related genes (Caspase 3, Caspase 8 and P53) (P < 0.05). The concentration of acetic acid and butyric acid in the cecum content of laying hens in the MCE + PBC group was significantly increased compared with the control group (P < 0.05). Conclusions: Collectively, dietary supplementation of 600 μg/kg MCE and 5 × 10⁸ CFU/kg compound Bacillus can improve laying performance by improving microbiota to enhance antioxidant capacity and intestinal barrier, regulate reproductive hormones and the concentration of cecal short-chain fatty acids of laying hens, and the combined effect of MCE and Bacillus is better than that of single supplementation.

Autophagy is a conserved proteolytic mechanism, which degrades and recycles damaged organs and proteins in cells to resist external stress. Probiotics could induce autophagy; however, its underlying molecular mechanisms remain elusive. Our previous study has found that BaSC06 could alleviate oxidative stress by inducing autophagy in rats. This research aimed to verify whether Bacillus amyloliquefaciens SC06 can induce autophagy to alleviate oxidative stress in IPEC-J2 cells, as well as explore its mechanisms. IPEC-J2 cells were first pretreated with 10⁸ CFU/mL BaSC06, and then were induced to oxidative stress by the optimal dose of diquat. The results showed that BaSC06 significantly triggered autophagy, indicated by the up-regulation of LC3 and Beclin1 along with downregulation of p62 in IPEC-J2 cells. Further analysis revealed that BaSC06 inhibited the AKT–FOXO signaling pathway by inhibiting the expression of p-AKT and p-FOXO and inducing the expression of SIRT1, resulting in increasing the transcriptional activity of FOXO3 and gene expression of the ATG5–ATG12 complex to induce autophagy, which alleviated oxidative stress and apoptosis. Taken together, BaSC06 can induce AKT–FOXO-mediated autophagy to alleviate oxidative stress-induced apoptosis and cell damage, thus providing novel theoretical support for probiotics in the prevention and treatment of oxidative damage.

Clostridium perfringens (C. perfringens) causes intestinal injury through overgrowth and the secretion of multiple toxins, leading to diarrhea and necrotic enteritis in animals, including pigs, chickens, and sheep. This study aimed to investigate the protective effects of Lactobacillus plantarum (L. plantarum) Lac16 on C. perfringens infection-associated injury in intestinal porcine epithelial cell line (IPEC-J2). The results showed that L. plantarum Lac16 significantly inhibited the growth of C. perfringens, which was accompanied by a decrease in pH levels. In addition, L. plantarum Lac16 significantly elevated the mRNA expression levels of host defense peptides (HDPs) in IPEC-J2 cells, decreased the adhesion of C. perfringens to IPEC-J2 cells, and attenuated C. perfringens-induced cellular cytotoxicity and intestinal barrier damage. Furthermore, L. plantarum Lac16 significantly suppressed C. perfringens-induced gene expressions of proinflammatory cytokines and pattern recognition receptors (PRRs) in IPEC-J2 cells. Moreover, L. plantarum Lac16 preincubation effectively inhibited the phosphorylation of p65 caused by C. perfringens infection. Collectively, probiotic L. plantarum Lac16 exerts protective effects against C. perfringens infection-associated injury in IPEC-J2 cells.