RESUMEN

This study was aimed to investigate the effects of yeast polysaccharides (YPS) on growth performance, intestinal health, and aflatoxin metabolism in livers of broilers fed diets naturally contaminated with mixed mycotoxins (MYCO). A total of 480 one-day-old Arbor Acre male broilers were randomly allocated into a 2 × 3 factorial arrangement of treatments (8 replicates with 10 birds per replicate) for 6 wk to assess the effects of 3 levels of YPS (0, 1, or 2 g/kg) on the broilers fed diets contaminated with or without MYCO (95 µg/kg aflatoxin B1, 1.5 mg/kg deoxynivalenol, and 490 µg/kg zearalenone). Results showed that mycotoxins contaminated diets led to significant increments in serum malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, mRNA expressions of TLR4 and 4EBP1 associated with oxidative stress, mRNA expressions of CYP1A1, CYP1A2, CYP2A6, and CYP3A4 associated with hepatic phase Ⅰ metabolizing enzymes, mRNA expressions of p53 associated with hepatic mitochondrial apoptosis, and AFB1 residues in the liver (P < 0.05); meanwhile dietary MYCO decreased the jejunal villus height (VH), villus height/crypt depth (VH/CD), the activity of serum total antioxidant capacity (T-AOC), mRNA expressions of jejunal HIF-1α, HMOX, and XDH associated with oxidative stress, mRNA expressions of jejunal CLDN1, ZO1, and ZO2, and mRNA expression of GST associated with hepatic phase Ⅱ metabolizing enzymes of broilers (P < 0.05). Notably, the adverse effects induced by MYCO on broilers were mitigated by supplementation with YPS. Dietary YPS supplementation reduced the concentrations of serum MDA and 8-OHdG, jejunal CD, mRNA expression of jejunal TLR2, and 4EBP1, hepatic CYP1A2, and p53, and the AFB1 residues in the liver (P < 0.05), and elevated the serum T-AOC and SOD, jejunal VH, and VH/CD, and mRNA expression of jejunal XDH, hepatic GST of broilers (P < 0.05). There were significant interactions between MYCO and YPS levels on the growth performance (BW, ADFI, ADG, and F/G) at d 1 to 21, d 22 to 42, and d 1 to 42, serum GSH-Px activity, and mRNA expression of jejunal CLDN2 and hepatic ras of broilers (P < 0.05). In contrast with MYCO group, the addition of YPS increased BW, ADFI, and ADG, the serum GSH-Px activity (14.31%-46.92%), mRNA levels of jejunal CLDN2 (94.39%-103.02%), decreased F/G, and mRNA levels of hepatic ras (57.83%-63.62%) of broilers (P < 0.05). In conclusion, dietary supplements with YPS protected broilers from mixed mycotoxins toxicities meanwhile keeping normal performance of broilers, presumably via reducing intestinal oxidative stress, protecting intestinal structural integrity, and improving hepatic metabolic enzymes to minimize the AFB1 residue in the liver and enhance the performance of broilers.

Asunto(s)

Micotoxinas , Saccharomyces cerevisiae , Masculino , Animales , Saccharomyces cerevisiae/metabolismo , Pollos/fisiología , Citocromo P-450 CYP1A2/metabolismo , Citocromo P-450 CYP1A2/farmacología , Micotoxinas/toxicidad , Micotoxinas/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Proteína p53 Supresora de Tumor/farmacología , Suplementos Dietéticos , Estrés Oxidativo , Dieta/veterinaria , Antioxidantes/metabolismo , Polisacáridos/farmacología , ARN Mensajero/metabolismo , Alimentación Animal/análisis

RESUMEN

Oxidation of food-derived phospholipids (PLs) can influence nutrient digestion and induce oxidative stress in gastrointestinal epithelium. In this study, hen egg yolk PL fraction was used to evaluate the effect of lipoxygenase (LOX)-induced PL oxidation on the rate of PL hydrolysis catalyzed by pancreatic phospholipase A2 (PLA2) in the presence of bile salts (BSs). Then, PL/BS solutions containing native or oxidized PLs were used in in vitro intestinal digestion to assess the effect of PL oxidation and hydrolysis on the toxicity towards HT29 cell line. Based on the obtained results, we suggest that hexanal and (E)-2-nonenal, formed by the decomposition of PL hydroperoxides, inhibited PLA2 activity. The cell exposure to simulated intestinal fluid (SIF) containing BSs decreased HT29 cell viability and significantly damaged cellular DNA. However, the genotoxic effect was reversed in the presence of all tested PL samples, while the protective effect against the BS-induced cytotoxicity was observed for native non-hydrolyzed PLs, but was not clearly visible for other samples. This can result from an overlap of other toxic effects such as lipotoxicity or disturbance of cellular redox homeostasis. Taking into account the data obtained, it was proposed that the PLA2 activity decline in the presence of PL oxidation products may be a kind of protective mechanism against rapid release of oxidized FAs characterized by high cytotoxic effect towards intestinal epithelium cells.

Asunto(s)

Pollos , Fosfolípidos , Humanos , Animales , Femenino , Fosfolípidos/metabolismo , Hidrólisis , Pollos/metabolismo , Fosfolipasas A2/toxicidad , Fosfolipasas A2/metabolismo , Oxidación-Reducción , Línea Celular , Mucosa Intestinal/metabolismo

RESUMEN

This study was conducted to investigate the alleviative effects of trans-anethole (TA) on intestinal oxidative stress by enhancing the activities of intestinal antioxidant enzymes and activating the Nrf2 signaling pathway in subclinical necrotic enteritis (NE) infected broilers. A total of 192 1-day-old male Arbor Acres broilers were randomly allocated into three treatment groups: (1) control (CON); (2) subclinical NE challenge (NE); (3) NE challenge + 600 mg/kg TA (NE+TA600). Subclinical NE was induced by oral administration of live coccidiosis vaccine containing 2 × 104 oocysts at 10 days of age and 2 ml of Clostridium perfringens type A solution (3 × 108 CFU/ml) daily from days 14 to 19. The results showed that NE infection led to a severe decline (p < 0.05) in the final body weight (BW) and average daily gain (ADG), but an increase (p < 0.05) in feed/gain (F/G) of broilers at day 10-21 and day 1-21 compared with the control group. TA administration improved (p < 0.05) the growth performance of NE birds. The intestinal villus height (VH) and villus height/crypt depth (VH/CD) were reduced (p < 0.05) by NE challenge as compared with those of the control group, which was elevated by TA administration. Subclinical NE infection decreased (p < 0.05) serum activities of total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), and jejunal and ileal glutathione peroxidase (GSH-PX), and T-SOD activity as well as T-AOC in the jejunum, while TA interventions positively elevated that (p < 0.05). Administration of TA protected the intestine against oxidative stress through up-regulation of intestinal nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway as compared with the NE group (p < 0.05). In addition, dietary inclusion of TA elevated (p < 0.05) mRNA abundance of c-mesenchymal-epithelial transition factor (c-Met), jejunal epidermal growth factor receptor (EGFR), and transforming growth factor-beta 1 (TGF-ß1) in the jejunum and ileum of birds after subclinical NE challenge. In conclusion, 600 mg/kg of TA may be a promising tool to prevent and control subclinical NE by increasing intestinal antioxidant status in broilers.

RESUMEN

Carrageenan oligosaccharides (COS) have been reported to possess excellent antioxidant activities, but the underlying mechanism remains poorly understood. In this study, H2O2 was applied to trigger oxidative stress. The results showed that the addition of COS could effectively extend the lifespan of female Drosophila, which was associated with improvements by COS on the antioxidant defense system, including a decrease in MDA, the enhanced activities of SOD and CAT, the reduction of ROS in intestinal epithelial cells, and the up-regulation of antioxidant-relevant genes (GCL, GSTs, Nrf2, SOD). Meanwhile, the axenic female Drosophila fed with COS showed almost no improvement in the above measurements after H2O2 treatment, which highlighted the antioxidant mechanism of COS was closely related to intestinal microorganisms. Then, 16S rDNA high-throughput sequencing was applied and the result showed that the addition of COS in diets contributed to the diversity and abundance of intestinal flora in H2O2 induced female Drosophila. Moreover, COS significantly inhibited the expression of gene mTOR, elevated its downstream gene 4E-BP, and further inhibited autophagy-relevant genes (AMPKα, Atg1, Atg5, Atg8a) in H2O2 induced female Drosophila. The inhibition of the mTOR pathway and the activation of autophagy was probably mediated by the antioxidant effects of COS. These results provide potential evidence for further understanding of COS as an intestinal antioxidant.

RESUMEN

This study aims to study the protective effect and mechanism of carnosol on intestinal oxidative stress. Porcine intestinal epithelial cells (ZYM-SIEC02) were pretreated with carnosol. Tert-butyl hydroperoxide (t-BHP) was added to stimulate the cells. The cell colonization and viability were detected by Edu staining, MTT, and cell counting kit-8 (CCK8) assays. The expressions of reactive oxygen species (ROS), nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA) in intracellular and oxidative stress were detected. The expression of related genes and proteins in cells was detected by real-time PCR and western blot. The regulatory mechanisms were identified by co-immunoprecipitation (Co-IP) and chromatin immunoprecipitation (CHIP) assays. The results showed that t-BHP reduced cell proliferation and viability, while cells pretreated with carnosol had resistance to t-BHP, decreased intracellular ROS, MDA and NO levels, and increased SOD content. The mRNA and protein levels of heme oxygenase 1/Nuclear respiratory factor 2 (HO-1/Nrf-2) in ZYM-SIEC02 cells treated with carnosol were significantly increased. Nrf2 was able to bind to cell cycle negative regulatory protein p21 Nrf2 could bind to the promoter regions of cyclin D1 (CCND1) and SOD genes. In conclusion, carnosol has a protective effect on intestinal epithelial cells by up-regulating the expression of Nrf2 and inhibiting p21 protein to promote the expression of CCND1 and SOD.