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A close interplay exists between the gut and liver, known as the "gut-liver axis", which plays a vital role in health and disease. This research aimed to explore the effects of dietary formic acid polymer (FAP) addition on inflammatory injury in gut-liver axis of broilers due to lipopolysaccharide (LPS) challenge. Four hundred and fifty 1-day-old male Arbor Acres broilers were assigned to three treatment groups: (1) control (non-challenged, basal diet); (2) LPS (LPS-challenged, basal diet); (3) LPS+FAP (LPS-challenged, basal diet with 1,000 mg/kg FAP). The trial lasted 21 days. On experimental days 17, 19, and 21, the LPS and LPS+FAP groups were intraperitoneally administered LPS (1 mg/kg BW), and the control group received an equal volume of physiological saline via intraperitoneal injection. Results showed that LPS injection induced inflammatory response, resulted in liver damage, and destroyed intestinal morphology and mucosal barrier. However, dietary FAP supplementation alleviated LPS-induced adverse effects on liver and small intestine by decreasing inflammatory response and suppressing cell death. In conclusion, supplementation of 1000 mg/kg FAP mitigated LPS-induced inflammatory injury in gut-liver axis in broilers.

Researches have shown that dietary zearalenone (ZEA) caused oxidative stress in the liver and reproductive organs of postweaning gilts. However, information on the effects of ZEA on oxidative stress of the small intestine in the piglets is limited. The objective of this study was to determine the effects of ZEA exposure on oxidative stress, the Kelch-like erythroid cell-derived protein with CNC homology (ECH)-associated protein 1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and on immunohistochemistry of the jejunum in postweaning gilts. A 35-d feeding experiment using 40 postweaning gilts (Landrace × Yorkshire × Duroc) with an average BW of 14.01 ± 0.86 kg in 4 groups fed corn-soybean meal-based diets containing 0, 0.5, 1.0, and 1.5 mg ZEA/kg was conducted. The jejunum was obtained at the end of the experiment and used for analyses. The results showed that the activities of total superoxide dismutase and glutathione peroxidase and the relative expressions of Keap1 mRNA and protein in the jejunum linearly and quadratically decreased (P < 0.05) with increasing concentrations of ZEA in the diets. The malondialdehyde content, the integrated optical density of Nrf2 and glutathione peroxidase 1 (GPX1), and the relative expressions of Nrf2, GPX1, quinone oxidoreductase 1 (NQO1), and modifier subunit of glutamate-cysteine ligase (GCLM) mRNA and proteins linearly and quadratically increased (P < 0.05) with increasing levels of ZEA. Immunohistochemical analysis showed that Nrf2 and GPX1 immunoreactivity was enhanced by the ZEA treatments, and block localization of yellow and brown immunoreactive substances in the jejunum was observed with increasing levels of ZEA. The results suggest that ingested ZEA induced oxidative stress in the jejunum in postweaning gilts through upregulation of the Keap1-Nrf2 signaling pathway and downstream target genes NQO1, HO1, and GCLM, indicating the important role of the Keap1-Nrf2 signaling pathway in oxidative stress induced by ZEA in the jejunum of the postweaning piglets.

Zearalenone (ZEN) is a nonsteroidal estrogenic mycotoxin produced by Fusariumstrains that is harmful to the intestinal health of animals and is widely present in contaminated crops. The objective of this study was to investigate the potential therapeutic target of ZEN-induced jejunal damage in weaned gilts. Sixteen weaned gilts either received a basal diet or a basal diet supplemented with 3.0 mg/kg ZEN in a 32-d experiment. The results showed that ZEN at the concentration of 3.0 mg/kg diet activated the inflammatory response and caused oxidative stress of gilts (P < 0.05). ZEN exposure resulted in the upregulation (P < 0.05) of the Exchange protein directly activated by the cAMP 1/Ras-related protein1/c-Jun N-terminal kinase (Epac1/Rap1/JNK) signaling pathway in the jejunum of gilts in vivo and in the intestinal porcine epithelial cells in vitro. The cell viability, EdU-positive cells, and the mRNA expression of B-cell lymphoma-2(Bcl-2) were decreased, whereas the reactive oxygen species production and the mRNA expressions of Bcl-2-associated X(Bax) and Cysteine-aspartic acid protease 3(Caspase3) were increased (P < 0.05) by ZEN. However, ZEN increased the mRNA expression of Bcl-2and decreased the mRNA expressions of Baxand caspase3(P < 0.05) after the Epac1 was blocked. These results collectively indicated that a 3.0 mg ZEN /kg diet induced jejunal damage via the Epac1/Rap1/JNK signaling pathway.The dietary supplementation of ZEN at 3.0 mg/kg was found to stimulate the inflammatory response and oxidative stress through the Epac1/Rap1/JNK signaling pathway in the jejunum of weaned gilts. The findings of this study indicate that targeting the Epac1/Rap1/JNK signaling pathway may represent a potential therapeutic approach to alleviating the detrimental effects of ZEN on the jejunal health of weaned gilts.Mycotoxins have caused huge economic losses to livestock industry. This study assessed the impact of zearalenone (ZEN) on the jejunum of weaned gilts. Results revealed that significant inflammatory response and oxidative stress were stimulated by 3.0 mg/kg ZEN in the jejunum tissue of weaned gilts. Furthermore, the reactive oxygen species accumulation and apoptosis in the intestinal porcine epithelial cells (IPEC-J2) were triggered, respectively. The negative impact of ZEN on the jejunum was by activation of Epac1/Rap1/JNK signaling pathway in the jejunum and this could be reduced by blocking Epac1. A more comprehensive understanding of the underlying molecular mechanisms will facilitate the development of novel strategies to mitigate the detrimental effect of ZEN on the jejunum of weaned gilts.Graphical Abstract

To investigate the effects of dietary supplementation of star anise oil (SAO) on performance and antioxidant status of laying hens, a total of 864 Hy-Line brown laying hens at 26 wk of age were randomly allocated to 4 treatments with 6 replicates of 36 birds. Dietary treatments were non-star anise oil supplementation and supplemented with SAO at the level of 200, 400, and 600 mg/kg diet. The birds were fed the diets for 56 d. Average egg weight, average daily feed intake (ADFI), egg mass, laying rate, and feed conversion of each replicate were measured. Blood and liver samples from 12 birds were obtained, 72 eggs were picked out, per treatment at day 28 and day 56 of the experiment, and eggs stored for 56 d, to determine antioxidant status in serum, liver, and yolk. All laying hens had similar average egg weight, egg mass, laying rate, and feed conversion in day 29 to day 56 or the entire period of the experiment but significant difference on ADFI in day 1 to day 56. However, increasing diet concentration of SAO tended to improve (P< 0.10) egg mass, average egg weight, and ADFI in day 1 to day 28. Supplementation of SAO linearly increased (P< 0.05) activities of total superoxide dismutase (T-SOD) (day 28 and day 56) and glutathione peroxidase (GSH-PX) (day 56) in serum, GSH-PX (day 28 and day 56) in liver and total antioxidant capacity (T-AOC) (day 56) in serum and liver, but linearly reduced (P< 0.05) concentrations of malondialdehyde (MDA) (day 28 and day 56) in liver. Supplementation of SAO linearly increased (P< 0.05) T-SOD activity at day 14 and day 28, reduced (P< 0.05) MDA concentration at day 42 and day 56 of the experiment in yolk. Increasing content of SAO linearly (P< 0.05) increased T-SOD activity in yolk of eggs stored at day 0, 14, 28, 42, and 56, decreased MDA content of eggs stored at day 42 and 56, whether laying hens fed diets for 28 or 56 d. Dietary supplementation of SAO enhanced laying performance and overall antioxidant status of laying hens in a dose-dependent manner.

This study was conducted to determine the effects of maternal dietary supplementation of ferrous glycine chelate (Fe-Gly) and ferrous sulfate monohydrate (FeSO4·H2O) on the relative organ weight, tissue iron contents, red blood cells (RBC), hemoglobin concentration (HGB) and hematocrit (HCT) in blood, as well as ferritin (Fn), serum iron (SI), and total iron binding capacity (TIBC) in serum of newborn piglets. Forty-five sows (Landrace × Large white, mean parity 3 to 4, no significant differences in BW) were randomly allotted to 9 treatments (n = 5 sows/treatment): control (basal diet with no Fe supplementation), the basal diet supplemented with 50, 80, 110 or 140 mg Fe/kg as Fe-Gly, and the basal diet supplemented with 50, 80, 110 or 140 mg Fe/kg as FeSO4·H2O. The neonatal piglets (n = 45) were used to determine the relative organ weight, tissue iron contents and blood biochemical indices. Compared with the control, the relative weight of spleen and kidney were significantly increased (P < 0.05) in the Fe-Gly groups. The iron contents in liver, spleen, kidney and femur were also found increased (P < 0.05) in the Fe-Gly groups. The RBC (d 1 and 21), HGB (d 1 and 21) and HCT (d 1 and 21) in blood and Fn (d 1) and SI (d 1 and 21) significantly increased (P < 0.05), but the TIBC (d 1 and 21) in serum decreased (P < 0.05) in the Fe-Gly groups. Moreover, the kidney relative weight, iron content in liver, spleen, kidney and femur, RBC (d 1) and HGB (d 21) in blood, and SI (d 1) in the Fe-Gly groups increased (P < 0.05) compared with the FeSO4·H2O treatment. Linear and quadratic responses of the kidney relative weight, the iron content in liver, spleen, kidney and femur, RBC (d 1 and 21), HGB (d 1 and 21) and HCT (d 1 and 21) in whole blood, SI (d 1) and TIBC (d 1 and 21) in the Fe-Gly groups were observed (P < 0.05). Linear responses of Fn (d 1 and 21) and SI (d 21) in the Fe-Gly groups, and spleen relative weight, HCT (d 1), Fn (d 1) and TIBC (d 1 and 21) in the FeSO4·H2O groups were observed (P < 0.05). These finding suggest that Fe-Gly supplemented at the level of 110 mg/kg in the diet of sows in this experiment is superior to other forms of supplementation, based on HGB concentration, the relative organ weight, tissue iron contents and blood biochemical indices of piglets.

Zearalenone (ZEA), an estrogenic mycotoxin, is produced mainly by Fusariumfungi. Previous studies have indicated that acute ZEA exposure induced various damages in different species; however, its transparent hematotoxicity in female piglets at dietary levels of 1.1 to 3.2 mg/kg has not been shown. The present study was conducted to investigate the effects of dietary ZEA (1.1–3.2 mg/kg) on hematology, T lymphocyte subset, immunoglobulin, antibody titer, lymphocyte proliferation rate (LPR), and interleukin-2 (IL-2) in peripheral blood of post-weaning gilts. A total of 20 female piglets (Landrace × Yorkshire × Duroc), weaned at 42 d with an average body weight of 10.36 ± 1.21 kg were used in the study. Female piglets were kept in a temperature controlled room, divided into four treatments, and fed a diet based on corn-soybean meal-fishmeal-whey, with an addition of 0, 1.1, 2.0, or 3.2 mg/kg purified ZEA for 18 d ad libitum. Feed intake and refusal were measured daily and individual pigs were weighed weekly. Blood and serum samples were collected for selected immunological measurements. Female piglets fed different levels of dietary ZEA grew similarly with no difference in feed intake. Hematological values including leukocytes, platelets, lymphocytes, hematocrit, and mean corpuscular hemoglobin (MCH) decreased linearly (P < 0.05) as dietary ZEA increased. Female piglets fed diets containing 2.0 mg/kg ZEA or greater showed significantly decreased CD4+CD8+, CD4+, and CD4+/CD8+in comparison to the control (P < 0.05), whereas CD8+was significantly increased (P = 0.026) in the gilts which were fed the diet containing 3.2 mg/kg ZEA. Serum immunoglobulin G (IgG) and the antibody titer on d 18 were reduced linearly as dietary ZEA levels increased (P < 0.001). Linear decrease in LPR was observed (P < 0.05). Female piglets fed diets containing 2.0 mg/kg ZEA or more showed significantly decreased IL-2 in comparison to the control (P < 0.05). The results suggested that dietary ZEA at the levels of 1.1 to 3.2 mg/kg can induce different degrees of hematotoxicity and negatively affect immune function in female piglets.

Alpha-linolenic acid (ALA), which is an n-3 polyunsaturated fatty acid (PUFA), influences honey bee feed intake and longevity. The objective of this study was to research the effect of six dietary ALA levels on the growth and development of Apis mellifera ligustica colonies. In the early spring, a total of 36 honey bee colonies of equal size and queen quality were randomly allocated into 6 groups. The six groups of honey bees were fed a basal diet with supplementation of ALA levels at 0 (group A), 2 (group B), 4 (group C), 6 (group D), 8 (group E), and 10% (group F). In this study, there were significant effects of pollen substitute ALA levels on the feeding amounts of the bee colony, colony population, sealed brood amount, and weight of newly emerged workers (P<0.05). The workers’ midgut Lipase (LPS) activity of group C was significantly lower than that of the other groups (P<0.01). The worker bees in groups B, C, and D had significantly longer lifespans than those in the other groups (P<0.05). However, when the diets had ALA concentrations of more than 6%, the mortality of the honey bees increased (P<0.01). These results indicate that ALA levels of 2 ~ 4% of the pollen substitute were optimal for maintaining the highest reproductive performance and the digestion and absorption of fatty acids in honey bees during the period of spring multiplication. Additionally, ALA levels of 2 ~ 6% of the pollen substitute, improved worker bee longevity.

This study aimed to investigate the effect of zearalenone (ZEA) exposure on follicular development in weaned gilts, and its mechanism based on the silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor-γ co-activator 1α (PGC-1α) signaling pathway. A total of 32 healthy female weaned piglets (Landrace × Yorkshire × Duroc) with an average body weight of 12.39 ± 0.24 kg were randomly allotted to a basal diet supplemented with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-d feeding test. Blood and ovarian samples were obtained at the end of the experiment to determine serum toxin concentrations, ovarian histology, and the expressions of proliferating cell nuclear antigen (PCNA) and SIRT1/PGC-1α signaling pathway-related genes. Results showed that the vulva area, serum concentrations of ZEA, α-zearalenol and β-zearalenol, the thickness of the growing follicular layer, and the diameter of the largest growing follicles, as well as the expressions of SIRT1, PGC-1α, estrogen-related receptor α (ERRα), ATP synthase subunit beta (ATP5B), and PCNA, increased linearly (P< 0.05) with increasing dietary ZEA, whereas the thickness of the primordial follicle layer decreased linearly (P< 0.05). Immunohistochemical analysis showed that the immunoreactive substances of SIRT1 and PGC-1α in the ovaries enhanced with the increasing dietary ZEA (P< 0.05). In addition, the thickness of the growing follicular layer and the diameter of the largest growing follicle were positively correlated with relative mRNA and protein expressions of SIRT1, PGC-1α, ERRα, ATP5B, and PCNA (P< 0.05). However, the thickness of the primordial follicle layer was negatively correlated with the mRNA and protein expression of SIRT1, PGC-1α, ERRα, ATP5B, and PCNA (P< 0.05). Interestingly, the 1.5 mg/kg ZEA treatment had highly hyperplastic follicles, whereas 3.0 mg/kg ZEA resulted in a large number of follicular atresia, which indicated that low-dose ZEA exposure accelerated follicular proliferation, while high-dose ZEA promoted follicular atresia, although the critical value interval needs further confirmation. Results provide a theoretical basis for finding the therapeutic target of ZEA-induced reproductive disorders in weaned gilts.Zearalenone (ZEA), an estrogenic fusariotoxin, existing in various grains and feedstuffs, could disrupt the endocrine and reproductive systems. However, the underlying mechanisms of ZEA-induced follicular development have not been fully elucidated. This study was to explore the effects and the possible molecular mechanisms of ZEA on follicular development. A total of 32 female weaned piglets were randomly allotted to a basal diet supplemented with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-d feeding test. The results showed that dietary ZEA increased the vulva area and serum toxin levels, and accelerated follicle development. Moreover, 1.5 and 3.0 mg/kg ZEA changed the expression of proliferating cell nuclear antigen (PCNA) and activated the silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor-γ co-activator 1α (PGC-1α) signaling pathway. Meanwhile, ZEA could promote follicle development by regulating PCNA expression through activation of the SIRT1/PGC-1α signaling pathway. The very significant contribution was that the proliferated follicles significantly increased with the increasing ZEA concentration when the ZEA in the diet was less than 1.5 mg/kg; however, atretic follicles significantly increased when the ZEA in the diet was 3.0 mg/kg. This study provides a theoretical basis for finding the therapeutic target of ZEA-induced reproductive disorders in weaned gilts.The mechanism of zearalenone-induced follicular development in weaned gilts was revealed by histological examination, immunohistochemistry, real-time quantitative RT-PCR, and western blot analysis.

Accumulating evidences indicate that plant extracts and probiotics are effective antioxidant substitutes which play important roles in animal production. However, the comparative study of the mechanism underlying the antioxidant property of Illicium verum extracts (IVE) and probiotics with added glucose oxidase (PGO) on piglets remains to be explored. This study evaluated the difference and the interaction effect of IVE and PGO on serum, liver, and jejunum antioxidant capacity of weaned piglets. A total of 32 weaned piglets (Duroc × Landrace × Yorkshire) at the age of 28 d with an average body weight of 14.96 ± 0.32 kg were randomly divided into four treatments with eight replicates per treatment in a 2 × 2 factorial arrangement. Treatments included basal diet (IVE-PGO-), basal diet + 1,000 mg/kg PGO (IVE-PGO+), basal diet + 500 mg/kg IVE (IVE+PGO-), and basal diet + 500 mg/kg IVE + 1,000 mg/kg PGO (IVE+PGO+). All the piglets were housed individually for the 42-d trial period after 7-d adaptation. The piglets were euthanized at the end of the experiment and the liver and jejunum samples were taken and subjected to immunohistochemistry, Western blotting, as well as antioxidant and qRT-PCR analysis. Significant interactions were observed between IVE and PGO for total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) in serum (42 d), liver, and jejunum; malondialdehyde (MDA) in serum (21 d); and mRNA and protein expression of kelch sample related protein-1 (Keap1) and nuclear factor erythroid-2 related factor (Nrf2)/Keap1 in the liver and jejunum (P < 0.05). Both IVE and PGO improved (P < 0.05) T-SOD and GSH-Px in the serum (42 d), liver, and jejunum, and the mRNA and protein expression of Nrf2 and Nrf2/Keap1 in the liver and jejunum, but decreased (P < 0.05) MDA in the serum (21 d) and the mRNA and protein expression of Keap1 in the liver and jejunum. Immunohistochemical results confirmed that IVE and PGO enhanced the positive reactions of Nrf2 but weakened Keap1 in both the liver and jejunum. In conclusion, the results confirmed that IVE (500 mg/kg) and PGO (1,000 mg/kg) can improve the antioxidant capacity of weaned piglets and that the interaction effect between IVE and PGO is significant. At the same time, the fact that IVE and PGO activate the Nrf2/Keap1 in the liver and jejunum signaling pathway suggests that they play an important role in the ameliorative antioxidant capacity of weaned piglets. Therefore, the combination of IVE and PGO could be recommended as a new potential alternative to antibiotics in piglets' diets.