Vitamin E and vitamin C supplementation improves antioxidant status and immune function in oxidative-stressed breeder roosters by up-regulating expression of GSH-Px gene.

This study aimed to evaluate the effects of vitamin C and vitamin E on antioxidant capacity and immune function in oxidative-stressed breeder roosters. One hundred twenty 45-week-old Lveyang black-boned breeder roosters were randomly assigned to 5 dietary treatments, including negative control group (NC), positive control group (PC), and 3 trial groups, which were fed the diets containing 300 mg/kg VC, 200 mg/kg VE, or 300 mg/kg VC and 200 mg/kg VE (VC+VE). At 47 wk of age, the positive control and trial groups were subcutaneously injected 3 times every other d with dexamethasone (DEX) 4 mg/kg of body weight, the negative control group was injected with saline. The experiment lasted for 35 d. The results showed that at 50 wk of age, average daily feed intake of birds challenged with DEX significantly increased (P < 0.05). During post-stress recovery period (52 wk of age), dietary supplemental VE or VC+VE notably increased body weight under oxidative stress (P < 0.01). Oxidative stress induced by DEX could significantly decrease superoxide dismutase (SOD), IgM, antibody titer of ND and mRNA expression of SOD or glutathion peroxidase activity (GSH-Px), increase serous malondialdehyde (MDA) (P < 0.05). Supplementation of VC or VE significantly decreased serous MDA, and increased SOD under oxidative stress (P < 0.05). Supplementation of VC or VE, or their combination significantly increased the relative expression of GSH-Px mRNA when compared to the oxidative-stressed control treatment (P < 0.05), whereas did not alleviate the relative expression of SOD mRNA (P > 0.05). Therefore, the results suggest that addition of 300 mg/kg VC, 200 mg/kg VE or their combination could improve antioxidant ability and immune performance in oxidative-stressed breeder roosters through up-regulating the expression of GSH-Px gene.

Effects of dietary threonine levels on growth performance, serum biochemical indexes, antioxidant capacities, and gut morphology in broiler chickens.

A dose-response experiment was conducted to investigate the impacts of dietary threonine (Thr) levels on growth performance, serum biochemical indices, antioxidant capacities, and gut morphology of broiler chickens. Four hundred and thirty-two 1-d-old commercial broilers were allocated to 4 treatments consisting of 6 replicates of 18 birds. The experimental treatments received the same Thr-deficient basal diet and were labeled as follows: 85%, 100%, 125%, and 150% of NRC (1994) recommendations. The results demonstrated that on 21 d and 42 d, average daily weight gain (ADG, 22 to 42 d, 0 to 42 d) increased quadratically or cubically as the inclusion of Thr increased, while feed conversion ratio (FCR, 0 to 21 d, 0 to 42 d) decreased quadratically or cubically as dietary Thr increase from 85% to 150%. Excess dietary Thr levels triggered plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. The concentrations of total protein (TP) and globulin (GLO) increased quadratically with increasing Thr level, and the highest concentrations of TP and GLO were obtained at the 125% Thr level. Moreover, the plasma uric acid (UA) concentration decreased linearly or quadratically with the increase in dietary Thr level. Likewise, the serum glutathione peroxidase (GSH-Px) and total superoxide dismutases (T-SOD) activities increased quadratically as dietary Thr increased, and the highest activity of GSH-Px was obtained at the 125% Thr level, while the highest T-SOD level occurred in the 100% Thr group. Gut morphology of birds showed significant response to different graded concentrations of Thr level. Villus height (VH), crypt depth (CD), and VH:CD ratio (VH/CD) were increased linearly or quadratically by Thr supplementation. Therefore, the present study suggests that the NRC (1994) recommendations Thr level that was optimum for growth performance, and 125% of the NRC (1994) recommendations Thr level had better effects on biochemical indices, antioxidant function, and gut morphology of broilers.

Effects of dietary supplementation of synbiotics on growth performance, intestinal morphology, sIgA content and antioxidant capacities of broilers.

Today, several strategies are being used to decrease the serious effects of antibiotics abuse on broilers industry and public health, among which synbiotics are one of the most promising antibiotic alternative. This study was undertaken to assess the effects of synbiotics, which composed of probiotics (Bacillus subtilis) and prebiotics (xylooligosaccharide and mannanoligosaccharide), on growth performance, intestinal morphology, sIgA content and antioxidant parameters of broilers. Four hundred and fifty one-day-old commercial Cobb48 broilers were assigned to five treatments consisting of six replicates of 15 birds each pen. Five dietary treatments include basal diets (control), basal diets plus antibiotics (4 mg/kg Xanthomycin), basal diets plus 1 g of probiotics B. subtilis product/kg of diets (4 × 108  cfu/kg), basal diets plus 150 mg/kg xylooligosaccharide (35%) and 1 g/kg mannanoligosaccharide (75%), and basal diets plus synbiotics (1 g of probiotics B. subtilis product/kg of diets (4 × 108  cfu/kg), 150 mg/kg xylooligosaccharide (35%) and 1 g/kg mannanoligosaccharide (75%). The results demonstrated that on 21 and 42 days, dietary supplementation of the synbiotics significantly increased daily weight gain (p < 0.05), feed efficiency (p < 0.05), the villus height and villus:crypt ratio in the duodenum, jejunum and ileum (p < 0.05), as well as intestinal mucosa sIgA content (p < 0.05), serum T-SOD activity (p < 0.05) and lysozyme content (p < 0.05), comparing with control group. In conclusion, synbiotics (B. subtilis and xylooligosaccharide and mannanoligosaccharide) is one of the safe and ideal dietary supplementations to increase broilers' growth performance by improving small intestinal morphology, sIgA content and antioxidant capabilities.

Participation of B-cell-activating factor receptors in the pathogenesis of immune thrombocytopenia.

UNLABELLED: ESSENTIALS: Dysfunctional B-cell-activating factor (BAFF) system is related to many autoimmune diseases. The regulatory functions of BAFF/BAFF receptors were investigated in an in vitro coculture system. Different regulatory roles of BAFF were investigated via different receptors in immune thrombocytopenia. The upregulated BAFF receptors on autoreactive lymphocytes lead to their hypersensitivity to BAFF. BACKGROUND: The pathogenesis of immune thrombocytopenia (ITP) remains enigmatic. B-cell-activating factor (BAFF) and its receptors (BAFF receptor [BAFF-R], transmembrane activator and calcium modulator and cyclophilin ligand interactor [TACI], and B-cell maturation antigen) play central roles in the integrated homeostatic regulation of lymphocytes. OBJECTIVES: To investigate the pathologic roles of BAFF receptors in regulating the bioactivities of lymphocytes in ITP. METHODS: An in vitro culture system was established by stimulating CD14(-) peripheral lymphocytes with platelet-preloaded dendritic cells in the presence of recombinant human BAFF (rhBAFF; 20 ng mL(-1)). The functions of BAFF receptors were specifically blocked with blocking antibodies. RESULTS: BAFF-R, besides prolonging the survival of B cells in both patients and healthy controls, prominently promoted the survival of CD8(+) T cells and the proliferation of B cells in patients with ITP. TACI, as a positive regulator, not only promoted the proliferation of CD4(+) and CD8(+) T cells, but also significantly enhanced the secretion of interleukin-4 in patients with ITP, but not in controls. Besides revealing the pathologic roles of BAFF receptors, these results also indicate that lymphocytes of patients with ITP have enhanced antiapoptotic or proliferative capacity as compared with those from healthy controls when exposed under similar stimulation of rhBAFF. Further study demonstrated that activated autoreactive B cells and CD4(+) T cells from patients with ITP showed significantly higher expression of BAFF-R or TACI than those from healthy controls. CONCLUSIONS: Both BAFF-R and TACI are pathogenic participants in ITP. Their dysregulated expression in patients with ITP may lead to hyperreactivity of activated autoreactive lymphocytes in response to rhBAFF, and thus is highly significant in the pathogenesis of ITP.