A combination of selenium and Bacillus subtilis improves the quality and flavor of meat and slaughter performance of broilers.

This study aimed to investigate the effects of the combination of selenium and Bacillus subtilis (Se-BS) on the quality and flavor of meat and slaughter performance of broilers. A total of 240 one-day-old Arbor Acres broilers were randomly allotted to four treatments of a basal diet supplemented with no selenium (control), sodium selenite (SS), BS, or Se-BS and raised for 42 days. Compared with the control group, Se-BS significantly increased the carcass weight, the half-eviscerated weight, the completely eviscerated weight, the carcass rate, and redness in broiler muscles; improved the antioxidant state by increasing glutathione peroxidase (GPx) and glutathione S-transferase activities, the total antioxidant capacity, and GPx-1 and thioredoxin reductase 1 messenger RNA (mRNA) levels; promoted biological activity by increasing the contents of glutamate, phenylalanine, lysine, and tyrosine; and increased Se and five types of nitrogenous volatile substances in muscles. On the other hand, Se-BS treatment decreased the shear force, drip loss, and the malondialdehyde, glutathione, and lead contents in muscles. Se-BS exerted a better effect on slaughter performance, the physicochemical quality of meat, the redox status, the amino acid contents, the trace element contents, and volatile substances compared with SS and BS. In conclusion, Se-BS had a positive effect on the quality and flavor of meat and slaughter performance of broilers, suggesting that Se-BS may be a beneficial feed additive.

Selenium-enriched Bacillus subtilis Improves Growth Performance, Antioxidant Capacity, Immune Status, and Gut Health of Broiler Chickens.

This study aimed to investigate the effects of selenium (Se)-enriched Bacillus subtilis (Se-BS) on growth performance, antioxidant capacity, immune status, and gut health in broilers. A total of 240 one-day-old Arbor Acres broilers were randomly allotted to four groups and fed with basal diet (control group), 0.30 mg/kg Se (SS group), 3 × 109 CFU/g B. subtilis (BS group), and 0.30 mg/kg Se + 3 × 109 CFU/g B. subtilis (Se-BS group) for 42 days. The results showed that Se-BS supplementation increased body weight (BW), average daily gain, the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and peroxidase (POD), total antioxidant capacity (T-AOC), and the contents of interleukin (IL)-2, IL-4, and immunoglobulin (Ig) G in plasma, the index and wall thickness of the duodenum, the villus height and crypt depth of the jejunum, and GPx-1 and thioredoxin reductase 1 mRNA levels in liver and intestine and decreased feed conversion ratio (FCR) and plasma malondialdehyde (MDA) content compared with the control group on day 42 (P < 0.05). Compared with groups SS and BS, Se-BS supplementation increased BW, the activities of GPx, CAT, and POD, and the contents of IL-2, IL-4, and IgG in plasma, the index and wall thickness of the duodenum, the crypt depth and secretory IgA content of the jejunum, and GPx-1 mRNA levels in liver and intestine and decreased FCR and plasma MDA content on day 42 (P < 0.05). In conclusion, Se-BS supplementation effectively improved the growth performance antioxidant capacity, immune status, and gut health of broilers.

Selenide Chitosan Sulfate Improved the Hepatocyte Activity, Growth Performance, and Anti-oxidation Capacity by Activating the Thioredoxin Reductase of Chickens In Vitro and In Vivo.

Chicken hepatocytes were cultured in vitro and 240 specific pathogen-free (SPF) white leghorns chickens (7 days old) were obtained. The hepatocytes and chickens were randomly allocated to one of six treatment groups: control group; chitosan (COS) group; sodium selenite (Na2SeO3) group; selenide chitosan (COS-Se) group; chitosan sulfate (LS-COS) group; and selenide chitosan sulfate (LS-COS-Se) group. Our results showed that LS-COS-Se increased (P < 0.05) the activities of thioredoxin reductase (TXNRD), anti-superoxide anion radical (antiO2-), and superoxide dismutase (SOD), the mRNA levels of thioredoxin reductase 1 (TXNRD1) and thioredoxin reductase 3 (TXNRD3), and the chicken body weight, but reduced (P < 0.05) the malondialdehyde (MDA) content and the lactate dehydrogenase (LDH) activity. Compared with COS and LS-COS, the LS-COS-Se treatment increased (P < 0.05) the activities of TXNRD, SOD, catalase (CAT), and the mRNA levels of TXNRD1 and TXNRD3, but reduced (P < 0.05) the MDA content in vitro, whereas, in vivo, it increased (P < 0.05) body weight on day 28; the activities of TXNRD, antiO2-, and SOD; and the mRNA levels of TXNRD1 and TXNRD3. Compared with Na2SeO3 and COS-Se, the LS-COS-Se treatment increased (P < 0.05) the TXNRD and SOD activities, the mRNA levels of TXNRD1 and TXNRD3 in vitro, increased (P < 0.05) the chicken body weight on day 28, and the TXNRD, antiO2-, and SOD activities, but reduced (P < 0.05) the MDA content. These results indicated that LS-COS-Se was a useful antioxidant that improved hepatocyte activity, growth performance, and anti-oxidation capacity in hepatocytes (in vitro) and SPF chicken (in vivo) by activating the TXNRD system.

Selenium-enriched Saccharomyces cerevisiae improves the meat quality of broiler chickens via activation of the glutathione and thioredoxin systems.

The aim of this study was to investigate the effects of selenium (Se)-enriched Saccharomyces cerevisiae (SSC) on meat quality and to elucidate the underlying mechanisms in broilers. A total of 200 one-day-old Arbor Acres broiler chickens were randomly allocated to one of four treatments with 5 replications of 10 chickens each. Group 1 served as a control and was fed a basal diet without Se supplementation, while groups 2, 3, and 4 were fed the basal diet supplemented with S. cerevisiae (SC), sodium selenite (SS), and SSC, respectively. Breast muscle samples were collected to evaluate meat quality, selenium concentration, oxidative stability, and the mRNA levels of antioxidant enzyme genes on day 42. As compared with groups 1 and 2, SS and SSC supplementation increased Se concentration, glutathione peroxidase (GPx) and thioredoxin reductase (TR) activities, total antioxidant capacity, and the mRNA levels of GPx-1, GPx-4, TR-1, and TR-3 (P < 0.05) and decreased drip loss and malondialdehyde (MDA) content (P < 0.05). As compared with group 3, SSC supplementation increased pH, lightness, yellowness, Se concentration, GPx and superoxide dismutase activities, and the mRNA levels of GPx-1 and GPx-4 (P < 0.05) but decreased drip loss and MDA content (P < 0.05). Thus, SSC improved meat quality and oxidative stability by activating the glutathione and thioredoxin systems, which should be attributed to the combined roles of Se and SC.

Effects of selenide chitosan sulfate on glutathione system in hepatocytes and specific pathogen-free chickens.

This study aimed to investigate the effects of selenide chitosan sulfate (Se-CTS-S) on glutathione (GSH) system in hepatocytes and chickens. Chitosan, sodium selenite (Na2SeO3), selenide chitosan, chitosan sulfate (CTS-S), and Se-CTS-S were added to the culture medium and the basal diets; glutathione peroxidase (GSH-Px) activity, GSH content, total antioxidant capacity (T-AOC), and mRNA levels of cellular GPx (GPx-1) and phospholipid hydroperoxide GPx (GPx-4) in vivo and in vitro were determined. The results showed that Se-CTS-S increased (P < 0.05) GPx-1 and GPx-4 mRNA levels in hepatocytes and livers, and GSH-Px activity, GSH content, and T-AOC in the medium, hepatocytes, plasma, and livers compared with the control and chitosan treatments. Compared with CTS-S, Se-CTS-S treatments increased (P < 0.05) GPx-1 and GPx-4 mRNA levels in hepatocytes and livers, and GSH-Px activity, GSH content, and T-AOC capacity in the medium, hepatocytes, and livers. Compared with Na2SeO3 and CTS-Se, Se-CTS-S increased (P < 0.05) GPx-1 mRNA levels in hepatocytes and livers, GPx-4 mRNA levels in hepatocytes and livers, GSH-Px activity in the medium, hepatocytes, and livers, GSH contents in plasma and livers, and T-AOC in the medium, plasma, and livers. Thus, Se-CTS-S showed better biological activity that mainly benefited from the synergistic effects of Se and sulfate on GSH system.

Effects of fermented feed on growth performance, immune response, and antioxidant capacity in laying hen chicks and the underlying molecular mechanism involving nuclear factor-κB.

This study investigated the effects of fermented-feed diets on growth performance, immune status, and antioxidant responses in laying hen chicks and the underlying molecular mechanism, specifically, the role of the nuclear factor-κB (NF-κB) signaling pathway. A total of 80 healthy 14-day-old laying hen chicks were randomly divided into 4 treatments: basal diet (CON); basal diet supplemented with 7.5% fermented feed (FD); FD diet plus the NF-κB inhibitor BAY 11-7082 (FD + BAY); and FD diet plus the NF-κB inhibitor JSH-23 (FD + JSH). The NF-κB inhibitors were administered by intraperitoneal injection. The experiment lasted 21 D. Fermented feed supplementation significantly increased the body weight and average body weight gain of laying hen chicks but significantly decreased the feed conversion ratio. Additionally, fermented feed supplementation significantly increased mitogen-activated T-cell and B-cell proliferation in the peripheral blood, as well as elevated the serum concentrations of interleukin (IL)-1, IL-2, IL-4, IL-6, and tumor necrosis factor (TNF-α); however, NF-κB inhibition significantly reduced T-cell proliferation and serum IL-1, IL-6, and TNF-α levels. The levels of IgA, IgG, IgM, and Newcastle disease virus antibody in the serum were significantly increased by the addition of fermented feed. Furthermore, fermented feed supplementation significantly improved antioxidant function, as indicated by the increases of total antioxidant capacity, total superoxide dismutase activity, and glutathione peroxidase activity and the decrease of malonaldehyde level. However, NF-κB inhibition reversed these changes. Western blot analysis showed that fermented feed treatment increased splenic IκB kinase ß and NF-κB protein levels, whereas these increases were prevented by NF-κB inhibition. In conclusion, fermented feed improves the growth performance, immune function, and antioxidant capacity of laying hen chicks. Fermented feed-induced modulation of T-cell proliferation, T helper type 1 and T helper type 2 cytokine production, and antioxidation is associated with NF-κB activation.

Stevioside inhibits inflammation and apoptosis by regulating TLR2 and TLR2-related proteins in S. aureus-infected mouse mammary epithelial cells.

Stevioside is a natural sweetener that is commonly used in traditional medicine and as a food additive. The object of this study was to investigate the anti-inflammatory and anti-apoptosis function of stevioside and the possible molecular mechanisms for such activity in Staphylococcus aureus (S. aureus)-infected mouse mammary epithelial cells (MMECs). The cells were treated with varying doses of stevioside before infection with S. aureus. The live/dead cells were detected by immunofluorescence microscopy. The pro-inflammatory cytokines were determined by ELISA. The mRNA of TLR2 and proteins related to NF-κB, MAPK and apoptosis were analyzed by q-PCR. The relative protein expression levels were determined by Western blot. The results indicated that stevioside inhibited the mRNA and protein expression of TNF-α, IL-6 and IL-1ß dose-dependently in S. aureus-stimulated MMECs. Stevioside suppressed the S. aureus-induced expression of TLR2 and proteins of the NF-κB and MAPK pathways as well as apoptosis. The mRNA levels of IκBα, p38, ERK, JNK, p65, caspase-3 and Bax were not influenced by the stevioside treatment. Stevioside exerts anti-inflammatory and anti-apoptotic properties by inhibiting the release of cytokines and the activation of TLR2 and proteins of the NF-κB and MAPK signaling pathways, as well as caspase-3 and Bax.

Stevioside plays an anti-inflammatory role by regulating the NF-κB and MAPK pathways in S. aureus-infected mouse mammary glands.

Mastitis is an inflammatory disease caused by microbial infection. Staphylococcus aureus is one of the primary bacteria responsible for mastitis. Stevioside is isolated from Stevia rebaudiana and is known to have therapeutic functions. This study was designed to evaluate the effects of stevioside in a mouse model of S. aureus-induced mastitis. In this study, the mouse mammary gland was infected with S. aureus to induce the mastitis model. The stevioside was administered intraperitoneally after the S. aureus infection was established. Hematoxylin-eosin (HE) staining, ELISA, Western blot, and q-PCR methods were used. The results show that stevioside significantly reduced the inflammatory cell infiltration and the levels of TNF-α, IL-1ß, and IL-6 and the respective expression of their messenger RNAs (mRNAs). Further studies revealed that stevioside downregulated the TLR2, NF-κB, and (mitogen-activated protein kinase) MAPK signaling pathways in the S. aureus-infected mouse mammary gland. Our results demonstrate that stevioside reduced the expression of TNF-α, IL-1ß, and IL-6 by inhibiting the phosphorylation of proteins in the NF-κB and MAPK signaling pathways dose-dependently, but that their mRNA expression was not obviously changed.