Curcumin Supplementation Improves Growth Performance and Anticoccidial Index by Improving the Antioxidant Capacity, Inhibiting Inflammatory Responses, and Maintaining Intestinal Barrier Function in Eimeria tenella-Infected Broilers.

This study was conducted to investigate the effects of dietary curcumin supplementation on growth performance, anticoccidial index, antioxidant capacity, intestinal inflammation, and cecum microbiota in broilers infected with Eimeria tenella. A total of 234 one-day-old broilers were categorized into three treatments, with six replicates per treatment containing 13 broilers each. The three treatments included the control group, Eimeria tenella group, and Eimeria tenella + curcumin (200 mg/kg) group. The feeding trial lasted for 42 days, during which the broilers were orally administered with 0.9% saline or 5 × 104Eimeria tenella oocysts on day 14 of the study. On day 17 and day 21, one bird per replicate was selected for slaughtering. Results indicated an increased survival rate and anticoccidial index and improved productive performance in coccidia-infected broilers with curcumin supplementation. Furthermore, curcumin enhanced the serum antioxidant capacity in Eimeria tenella-infected broilers, evidenced by increased serum catalase activity (3d, 7d), as well as decreased malondialdehyde level (3d, 7d) and nitric oxide synthase activity (7d) (p < 0.05). Curcumin also improved intestinal inflammation and barrier function, evidenced by the downregulation of interleukin (IL)-1ß (3d, 7d), TNF-alpha (TNF-α) (3d, 7d), and IL-2 (7d) and the up-regulated mRNA levels of claudin-1 (7d), zonula occludens (ZO-1; 3d, 7d), and occludin (3d, 7d) in the ceca of infected broilers (p < 0.05). Eimeria tenella infection significantly disrupted cecum microbial balance, but curcumin did not alleviate cecum microbial disorder in broilers infected with Eimeria tenella. Collectively, curcumin supplementation enhanced growth performance and anticoccidial index in Eimeria tenella-infected broilers via improving antioxidant ability and cecum inflammation without affecting cecum microbiota.

Deoxynivalenol and T-2 toxin cause liver damage and egg quality degradation through endoplasmic reticulum stress in summer laying hens.

The present study aimed to find whether low doses of mixed mycotoxins would affect egg quality in laying hens, and to explore the oxidative stress induced liver damage through endoplasmic reticulum during summer stress. A total of 96 Jinghong laying hens, 36 wks of age, were divided into four treatments, with eight repetitions per treatment and three hens per repetition. All the hens were raised in summer (average temperature: 31.3 ± 0.5℃; average humidity: 85.5 ± 0.2%) for 28d. One treatment was fed a basal diet as control (CON), and the other three treatments were fed the same diets containing 3.0 mg/kg deoxynivalenol (DON), 0.5 mg/kg T-2 toxin (T-2), and 1.5 mg/kg DON + 0.25 mg/kg T-2 toxin (Mix). Albumen height and Haugh unit were decreased (P < 0.05) in the Mix group on day 14 and 28. The activity of total antioxidant capacity, glutathione peroxidase, catalase, and superoxide dismutase were decreased (P < 0.05) in the DON, T-2, and Mix groups. The alkaline phosphatase level in DON, T-2, and Mix groups was significantly increased (P < 0.05). The level of interleukin-1ß, interferon-γ, and tumor necrosis factor-α in the Mix group were higher (P < 0.05) than CON, DON, and T-2 groups. Mix group upregulated the mRNA expressions of protein kinase RNA-like ER kinase, activating transcription factor4, IL-1ß, nuclear factor-κ-gene binding, and nuclear respiratory factor 2 in the liver (P < 0.05). The results showed that low doses of DON and T-2 toxin could cause oxidative stress in the liver, but DON and T-2 toxin have a cumulative effect on virulence, which can reduce egg quality and cause endoplasmic reticulum stress in the liver.

Intrauterine Growth Restriction Affects Colonic Barrier Function via Regulating the Nrf2/Keap1 and TLR4-NF-κB/ERK Pathways and Altering Colonic Microbiome and Metabolome Homeostasis in Growing-Finishing Pigs.

Intrauterine growth restriction (IUGR) pigs are characterized by long-term growth failure, metabolic disorders, and intestinal microbiota imbalance. The characteristics of the negative effects of IUGR at different growth stages of pigs are still unclear. Therefore, this study explored through multi-omics analyses whether the IUGR damages the intestinal barrier function and alters the colonization and metabolic profiles of the colonic microbiota in growing-finishing pigs. Seventy-two piglets (36 IUGR and 36 NBW) were allocated for this trial to analyze physiological and plasma biochemical parameters, as well as oxidative damage and inflammatory response in the colon. Moreover, the colonic microbiota communities and metabolome were examined using 16s rRNA sequencing and metabolomics technologies to reveal the intestinal characteristics of IUGR pigs at different growth stages (25, 50, and 100 kg). IUGR altered the concentrations of plasma glucose, total protein, triglycerides, and cholesterol. Colonic tight junction proteins were markedly inhibited by IUGR. IUGR decreased plasma T-AOC, SOD, and GSH levels and colonic SOD-1, SOD-2, and GPX-4 expressions by restraining the Nrf2/Keap1 signaling pathway. Moreover, IUGR increased colonic IL-1ß and TNF-α levels while reducing IL-10, possibly through activating the TLR4-NF-κB/ERK pathway. Notably, IUGR pigs had lower colonic Streptococcus abundance and Firmicutes-to-Bacteroidetes ratio at the 25 kg BW stage while having higher Firmicutes abundance at the 100 kg BW stage; moreover, IUGR pigs had lower SCFA concentrations. Metabolomics analysis showed that IUGR increased colonic lipids and lipid-like molecules, organic acids and derivatives, and organoheterocyclic compounds concentrations and enriched three differential metabolic pathways, including linoleic acid, sphingolipid, and purine metabolisms throughout the trial. Collectively, IUGR altered the nutrient metabolism, redox status, and colonic microbiota community and metabolite profiles of pigs and continued to disrupt colonic barrier function by reducing antioxidant capacity via the Nrf2/Keap1 pathway and activating inflammation via the TLR4-NF-κB/ERK pathway during the growing-finishing stage. Moreover, colonic Firmicutes and Streptococcus could be potential regulatory targets for modulating the metabolism and health of IUGR pigs.

Selenomethionine Supplementation Mitigates Liver Dysfunction, Oxidative Injury and Apoptosis through Enhancing Antioxidant Capacity and Inhibiting JNK MAPK Pathway in Piglets Fed Deoxynivalenol-Contaminated Diets.

This research evaluated the impacts of selenomethionine (Se-Met) on hepatic functions, oxidative stress, mitochondrial function, and apoptosis of piglets fed deoxynivalenol (DON)-contaminated diets. Twenty-four piglets were allocated four dietary treatments (n = 6) in a 28-day feeding trial. The four treatments included the control group, which received 0.3 mg/kg of Se (as Se-Met) without DON treatment, and the DON treatment groups received 0, 0.3, or 0.5 mg/kg Se as Se-Met. A dietary addition of 0.5 mg/kg Se improved liver pathology and reduced serum aspartate aminotransferase and lactate dehydrogenase levels in piglets fed DON-contaminated diets. Furthermore, 0.5 mg/kg Se mitigated the oxidative stress and apoptosis of piglets fed DON-contaminated diets, as indicated by the decreased reactive oxygen species level, and the down-regulated mRNA levels of NRF-1, Bax, and CASP9 in the liver. Importantly, 0.5 mg/kg Se enhanced the hepatic antioxidant capacity, as evidenced by increased hepatic total antioxidant capacity, catalase, glutathione peroxidase, and total superoxide dismutase activities, as well as the up-regulated mRNA levels of Nrf2, Gclm, NQO1, SOD1, and GPX1 in the liver. Moreover, 0.5 mg/kg Se down-regulated the p-JNK protein level in the liver of piglets fed DON-contaminated diets. Collectively, Se-Met supplementation mitigated liver dysfunction, oxidative injury, and apoptosis through enhancing antioxidant capacity and inhibiting the JNK MAPK pathway in piglets fed DON-contaminated diets.

Selenomethionine Alleviates Deoxynivalenol-Induced Oxidative Injury in Porcine Intestinal Epithelial Cells Independent of MAPK Pathway Regulation.

Deoxynivalenol (DON) is a prevalent contaminant in feed and food, posing a serious threat to the health of both humans and animals. The pig stands as an ideal subject for the study of DON due to its recognition as the most susceptible animal to DON. In this study, the IPEC-J2 cells were utilized as an in vitro model to explore the potential of SeMet in alleviating the intestinal toxicity and oxidative injury in intestinal epithelial cells when exposed to DON. Cells were treated either with or without 4.0 µM SeMet, in combination with or without a simultaneous treatment with 0.5 µg/mL DON, for a duration of 24 h. Then, cells or related samples were analyzed for cell proliferation, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) level, gene expressions, and protein expressions. The results showed that SeMet mitigated the cellular toxicity caused by DON, evidenced by elevated cell proliferation and the reduced LDH release of IPEC-J2 cells in the SeMet + DON group vs. the DON group. Moreover, the SeMet treatment markedly promoted antioxidant functions and decreased the oxidative injury in IPEC-J2 cell, which is indicated by the decreased ROS level and up-regulated mRNA levels of GPX1, TXNRD1, Nrf2, and GCLC in IPEC-J2 cells in the SeMet + DON group vs. the DON group. However, in both the absence and presence of exposure to DON, the SeMet treatment did not affect the protein expression of MAPK (JNK, Erk1/2, and P38) and phosphorylated MAPK (p-JNK, p-Erk1/2, and p-P38) in IPEC-J2 cells. Collectively, SeMet alleviated the DON-induced oxidative injury in porcine intestinal epithelial cells independent of the MAPK pathway regulation.

Dietary protein restriction regulates skeletal muscle fiber metabolic characteristics associated with the FGF21-ERK1/2 pathway.

Under conditions of dietary amino acid balance, decreasing the dietary crude protein (CP) level in pigs has a beneficial effect on meat quality. To further elucidate the mechanism, we explored the alteration of muscle fiber characteristics and key regulators related to myogenesis in the skeletal muscle of pigs fed a protein restricted diet. Compared to pigs fed a normal protein diet, dietary protein restriction significantly increased the slow-twitch muscle fiber proportion in skeletal muscle, succinic dehydrogenase (SDH) activity, the concentrations of ascorbate, biotin, palmitoleic acid, and the ratio of s-adenosylhomocysteine (SAM) to s-adenosylhomocysteine (SAH), but the fast-twitch muscle fiber proportion, lactate dehydrogenase (LDH) activity, the concentrations of ATP, glucose-6-phosphate, SAM, and SAH in skeletal muscle, and the ratio of serum triiodothyronine (T3) to tetraiodothyronine (T4) were decreased. In conclusion, we demonstrated that dietary protein restriction induced skeletal muscle fiber remodeling association the regulation of FGF21-ERK1/2-mTORC1 signaling in weaned piglets.

Effects of selenium-enriched yeast dietary supplementation on egg quality, gut morphology and caecal microflora of laying hens.

Selenium (Se) is an essential micronutrient for humans and animals and is a powerful antioxidant that can promote reproductive and immune functions. The purpose of this study was to evaluate the effects of supplemental dietary selenium-enriched yeast (SeY) on egg quality, gut morphology and microflora in laying hens. In total, 100 HY-Line Brown laying hens (45-week old) were randomly allocated to two groups with 10 replicates and fed either a basal diet (without Se supplementation) or a basal diet containing 0.2 mg/kg Se in the form of SeY for 8 weeks. The Se supplementation did not have a significant effect on egg quality and intestinal morphology of laying hens. Based on the 16S rRNA sequencing, SeY dietary supplementation effectively modulated the cecal microbiota structure. An alpha diversity analysis demonstrated that birds fed 100 mg/kg SeY had a higher cecal bacterial diversity. SeY dietary addition elevated Erysipelotrichia (class), Lachnospiraceae (family), Erysipelotrichaceae (family) and Ruminococcus_torques_group (genus; p < .05). Analysis of microbial community-level phenotypes revealed that SeY supplementation decreased the microorganism abundance of facultatively anaerobic and potentially pathogenic phenotypes. Overall, SeY supplementation cannot significantly improve intestinal morphology; however, it modulated the composition of cecal microbiota toward a healthier gut.

Fibroblast growth factor 21: An emerging pleiotropic regulator of lipid metabolism and the metabolic network.

Fibroblast growth factor 21 (FGF21) was originally identified as an important metabolic regulator which plays a crucial physiological role in regulating a variety of metabolic parameters through the metabolic network. As a novel multifunctional endocrine growth factor, the role of FGF21 in the metabolic network warrants extensive exploration. This insight was obtained from the observation that the FGF21-dependent mechanism that regulates lipid metabolism, glycogen transformation, and biological effectiveness occurs through the coordinated participation of the liver, adipose tissue, central nervous system, and sympathetic nerves. This review focuses on the role of FGF21-uncoupling protein 1 (UCP1) signaling in lipid metabolism and how FGF21 alleviates non-alcoholic fatty liver disease (NAFLD). Additionally, this review reveals the mechanism by which FGF21 governs glucolipid metabolism. Recent research on the role of FGF21 in the metabolic network has mostly focused on the crucial pathway of glucolipid metabolism. FGF21 has been shown to have multiple regulatory roles in the metabolic network. Since an adequate understanding of the concrete regulatory pathways of FGF21 in the metabolic network has not been attained, this review sheds new light on the metabolic mechanisms of FGF21, explores how FGF21 engages different tissues and organs, and lays a theoretical foundation for future in-depth research on FGF21-targeted treatment of metabolic diseases.

Neonatal resveratrol administration promotes skeletal muscle growth and insulin sensitivity in intrauterine growth-retarded suckling piglets associated with activation of FGF21-AMPKα pathway.

BACKGROUND: Skeletal muscle is a major insulin-sensitive tissue with a pivotal role in modulating glucose homeostasis. This study aimed to investigate the effect of resveratrol (RES) intervention during the suckling period on skeletal muscle growth and insulin sensitivity of neonates with intrauterine growth retardation (IUGR) in a pig model. RESULTS: Twelve pairs of normal birth weight (NBW) and IUGR neonatal male piglets were selected. The NBW and IUGR piglets were fed basal formula milk diet or identical diet supplemented with 0.1% RES from 7 to 21 days of age. Myofiber growth and differentiation, inflammation and insulin sensitivity in skeletal muscle were assessed. Early RES intervention promoted myofiber growth and maturity in IUGR piglets by ameliorating the myogenesis process and increasing thyroid hormone level. Administering RES also reduced triglyceride concentration in skeletal muscle of IUGR piglets, along with decreased inflammatory response, increased plasma fibroblast growth factor 21 (FGF21) concentration and improved insulin signaling. Meanwhile, the improvement of insulin sensitivity by RES may be partly regulated by activation of the FGF21/AMP-activated protein kinase α/sirtuin 1/peroxisome proliferator activated receptor-γ coactivator-1α pathway. CONCLUSION: Our results suggest that RES has beneficial effects in promoting myofiber growth and maturity and increasing skeletal muscle insulin sensitivity in IUGR piglets, which open a novel field of application of RES in IUGR infants for improving postnatal metabolic adaptation. © 2023 Society of Chemical Industry.

Fibroblast Growth Factor 21: A Fascinating Perspective on the Regulation of Muscle Metabolism.

Fibroblast growth factor 21 (FGF21) plays a vital role in normal eukaryotic organism development and homeostatic metabolism under the influence of internal and external factors such as endogenous hormone changes and exogenous stimuli. Over the last few decades, comprehensive studies have revealed the key role of FGF21 in regulating many fundamental metabolic pathways, including the muscle stress response, insulin signaling transmission, and muscle development. By coordinating these metabolic pathways, FGF21 is thought to contribute to acclimating to a stressful environment and the subsequent recovery of cell and tissue homeostasis. With the emphasis on FGF21, we extensively reviewed the research findings on the production and regulation of FGF21 and its role in muscle metabolism. We also emphasize how the FGF21 metabolic networks mediate mitochondrial dysfunction, glycogen consumption, and myogenic development and investigate prospective directions for the functional exploitation of FGF21 and its downstream effectors, such as the mammalian target of rapamycin (mTOR).

Effects of dietary tryptophan supplementation on rectal temperature, humoral immunity, and cecal microflora composition of heat-stressed broilers.

This trial aimed to determine the effects of tryptophan (Trp) on the rectal temperature, hormone, humoral immunity, and cecal microflora composition in broiler chickens under heat stress (HS). One hundred and eighty 18 days-old female Arbor Acres broilers were randomly divided into three treatment groups, with six replicates of ten birds in each replicate. The broilers were either raised under thermoneutral conditions (TN, 23 ± 1°C) or subjected to heat stress (34 ± 1°C for 8 h daily). The TN group received a basal diet, and another two heat-stressed groups were fed the basal diet (HS) or the basal diet supplemented with 0.18% Trp (HS + 0.18% Trp) for 21 consecutive days. The basal diet contained 0.18% Trp. Results revealed that HS increased the rectal temperature, serum epinephrine (EPI), and corticotropin-releasing hormone (CRH) concentrations (p < 0.05), reduced the bursal index, the levels of serum immunoglobulin A (IgA), IgG, IgM, and serotonin (5-HT) as well as the relative abundance of Actinobacteria in cecum (p < 0.05) compared with the TN group. Dietary supplementation of Trp decreased the rectal temperature, serum dopamine (DA), EPI, and the levels of CRH and L-kynurenine (p < 0.05), increased the bursal index, the levels of serum IgA, IgM, and 5-HT as well as the relative abundance of Ruminococcus torques group in cecum of heat-stressed broilers (p < 0.05) compared to HS group. In conclusion, dietary Trp supplementation decreased rectal temperature, improved cecal microbiota community and Trp metabolism, and enhanced humoral immunity of heat-stressed broilers.

A Critical Review of Kaempferol in Intestinal Health and Diseases.

Kaempferol, a secondary metabolite found in plants, is a naturally occurring flavonoid displaying significant potential in various biological activities. The chemical structure of kaempferol is distinguished by the presence of phenyl rings and four hydroxyl substituents, which make it an exceptional radical scavenger. Most recently, an increasing number of studies have demonstrated the significance of kaempferol in the regulation of intestinal function and the mitigation of intestinal inflammation. The focus of the review will primarily be on its impact in terms of antioxidant properties, inflammation, maintenance of intestinal barrier function, and its potential in the treatment of colorectal cancer and obesity. Future research endeavors should additionally give priority to investigating the specific dosage and duration of kaempferol administration for different pathological conditions, while simultaneously conducting deeper investigations into the comprehensible mechanisms of action related to the regulation of aryl hydrocarbon receptor (AhR). This review intends to present novel evidence supporting the utilization of kaempferol in the regulation of gut health and the management of associated diseases.

Research Progress on Lycopene in Swine and Poultry Nutrition: An Update.

Oxidative stress and in-feed antibiotics restrictions have accelerated the development of natural, green, safe feed additives for swine and poultry diets. Lycopene has the greatest antioxidant potential among the carotenoids, due to its specific chemical structure. In the past decade, increasing attention has been paid to lycopene as a functional additive for swine and poultry feed. In this review, we systematically summarized the latest research progress on lycopene in swine and poultry nutrition during the past ten years (2013-2022). We primarily focused on the effects of lycopene on productivity, meat and egg quality, antioxidant function, immune function, lipid metabolism, and intestinal physiological functions. The output of this review highlights the crucial foundation of lycopene as a functional feed supplement for animal nutrition.

Plant-derived polyphenols in sow nutrition: An update.

Oxidative stress is a potentially critical factor that affects productive performance in gestating and lactating sows. Polyphenols are a large class of plant secondary metabolites that possess robust antioxidant capacity. All polyphenols are structurally characterized by aromatic rings with multiple hydrogen hydroxyl groups; those make polyphenols perfect hydrogen atoms and electron donors to neutralize free radicals and other reactive oxygen species. In the past decade, increasing attention has been paid to polyphenols as functional feed additives for sows. Polyphenols have been found to alleviate inflammation and oxidative stress in sows, boost their reproductivity, and promote offspring growth and development. In this review, we provided a systematical summary of the latest research advances in plant-derived polyphenols in sow nutrition, and mainly focused on the effects of polyphenols on the (1) antioxidant and immune functions of sows, (2) placental functions and the growth and development of fetal piglets, (3) mammary gland functions and the growth and development of suckling piglets, and (4) the long-term growth and development of progeny pigs. The output of this review provides an important foundation, from more than 8,000 identified plant phenols, to screen potential polyphenols (or polyphenol-enriched plants) as functional feed additives suitable for gestating and lactating sows.

Polysaccharide-rich fractions from Enteromorpha prolifera improve hepatic steatosis and gut barrier integrity in high-fat diet-induced obese mice linking to modulation of gut microbiota.

Polysaccharides from Enteromorpha prolifera (EP) possess important benefits in the management of obesity and associated metabolic diseases, but to date, the underlying mechanism linking this alleviative effect of EP to gut microbiota remains obscure. This study aimed to investigate the effects of EP in improving lipid metabolism disorders and intestinal barrier disruption in mice with high-fat diet (HFD), and its association with modulation of gut microbiota. C57BL/6 mice were fed a control diet or a HFD with or without 5% EP for 12 weeks. Factors related to lipid metabolism, insulin signaling and intestinal barrier integrity, as well as the involvement of gut microbiota and metabolites, were measured. EP supplementation reduced HFD-induced adiposity and mitigated insulin resistance, hepatic steatosis and elevation of serum lipopolysaccharides (LPS). HFD impaired intestinal barrier integrity while improved due to EP. Moreover, EP administration ameliorated HFD-induced gut dysbiosis, as revealed by the increased short-chain fatty acid (SCFA)-producing bacteria (e.g., Bacteroides, Parabacteroides, Alloprevotella, and Ruminococcus) and gut barrier-protective Akkermansia muciniphila and decreased endotoxin-producing bacteria (e.g., Desulfovibrionaceae and Bilophila), accompanied by enrichment in intestinal SCFA content and reduction in circulating LPS level. The change of dominant bacterial genera is significantly correlated with improved metabolic profiles and intestinal permeability induced by EP. In conclusion, our results indicate that EP can attenuate HFD-induced metabolic disorders along with restoration of gut barrier integrity and lowering of circulating endotoxin, and these improvements are associated with modulation of gut microbiota composition and related metabolites. These data deepen mechanistic understanding of the anti-obesity and metabolic improving effects of EP.

Dietary glycine supplementation prevents heat stress-induced impairment of antioxidant status and intestinal barrier function in broilers.

This study tested the hypothesis that glycine improves intestinal barrier function through regulating oxidative stress in broilers exposed to heat stress. A total of 300 twenty-one-day-old female Arbor Acres broilers (600 ± 2.5g) was randomly allocated to 5 treatments (6 replicate of 10 birds each). The 5 treatments were as follows: the control group (CON) was kept under thermoneutral condition (24 ± 1°C) and was fed a basal diet. Broilers fed a basal diet and reared under high ambient temperature (HT) were considered as the HT group (34 ± 1°C for 8 h/d). Broilers fed a basal diet supplemented with 0.5%, 1.0%, and 2.0% glycine and exposed to HT were regarded as the HT + glycine treatments. The results exhibited that heat stress reduced growth performance, serum total antioxidant capacity (T-AOC), and glutathione (GSH) concentration (P < 0.05); increased activity of serum catalase (CAT) and the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) (P < 0.05). HT exposure led to downregulating the mRNA expression of NAD(P)H quinone dehydrogenase 1 (NQO1), Occludin, and zonula occludens-1 (ZO-1) (P < 0.05); enhanced the mRNA levels of Kelch-like ECH-associated protein 1 (Keap1), CAT, glutathione synthetase (GSS), and glutamate-cysteine ligase modifier subunit (GCLM) (P < 0.05); impaired the intestinal morphology (P < 0.05); and altered the diversity and community of gut microbiota (P < 0.05). The final body weight (FBW), ADFI, ADG, and gain-to-feed ratio (G: F) increased linearly or quadratically, and the antioxidant capacity was improved (P < 0.05) with glycine supplementation. Glycine treatment increased the villus height (VH), and villus height to crypt depth ratio (V/C) of the duodenum linearly or quadratically, and linearly increased the VH of jejunum and ileum. The mRNA expression of Occludin, and ZO-1 were increased linearly in the ileum mucosa of broilers subjected to HT. Collectively, these results demonstrated that glycine supplementation alleviates heat stress-induced dysfunction of antioxidant status and intestinal barrier in broilers.

A blend of formic acid, benzoic acid, and tributyrin alleviates ETEC K88-induced intestinal barrier dysfunction by regulating intestinal inflammation and gut microbiota in a murine model.

This study aimed to investigate the effects of an organic acid (OA) blend on intestinal barrier function, intestinal inflammation, and gut microbiota in mice challenged with enterotoxigenic Escherichia coli K88 (ETEC K88). Ninety female Kunming mice (7 weeks old) were randomly allotted to five treatments with six replicates per treatment and three mice per replicate. The five treatments were composed of the non-ETEC K88 challenge group and ETEC K88 challenge + OA blend groups (0, 0.6 %, 1.2 %, and 2.4 % OA blend). The OA blend consisted of 47.5 % formic acid, 47.5 % benzoic acid, and 5 % tributyrin. The feeding trial lasted for 15 days, and mice were intraperitoneally injected with PBS or ETEC K88 solution on day 15. At 24 h post-challenge, one mouse per replicate was selected for sample collection. The results showed that a dosage of 0.6 % OA blend alleviated the ETEC K88-induced intestinal barrier dysfunction, as indicated by the elevated villus height and the ratio of villus height to crypt depth of jejunum, and the reduced serum diamine oxidase (DAO) and D-lactate levels, as well as the up-regulated mRNA levels of ZO-1, Claudin-1, and Occludin in jejunum mucosa of mice. Furthermore, dietary addition with 0.6 % OA blend decreased ETEC K88-induced inflammation response, as suggested by the decreased TNF-α and IL-6 levels, and the increased IgA level in the serum, as well as the down-regulated mRNA level of TNF-α, IL-6, IL-1ß, TLR-4, MyD88, and MCP-1 in jejunum mucosa of mice. Regarding gut microbiota, the beta-diversity analysis revealed a remarkable clustering between the 0.6 % OA blend group and the ETEC K88 challenge group. Supplementation of 0.6 % OA blend decreased the relative abundance of Firmicutes, and increased the relative abundance of Bacteroidota, Desulfobacterota, and Verrucomicrobiota of colonic digesta in mice. Also, the butyric acid content in the colonic digesta of mice was increased by dietary 0.6 % OA blend supplementation. Collectively, a dosage of 0.6 % OA blend could alleviate the ETEC K88-induced intestinal barrier dysfunction by regulating intestinal inflammation and gut microbiota of mice.

Plant-Derived Polyphenols as Nrf2 Activators to Counteract Oxidative Stress and Intestinal Toxicity Induced by Deoxynivalenol in Swine: An Emerging Research Direction.

The contamination of deoxynivalenol (DON) in feed is a global problem, which seriously threatens the productivity efficiency and welfare of farm animals and the food security of humans. Pig is the most sensitive species to DON, and is readily exposed to DON through its grain-enriched diet. The intestine serves as the first biological barrier to ingested mycotoxin, and is, therefore, the first target of DON. In the past decade, a growing amount of attention has been paid to plant-derived polyphenols as functional compounds against DON-induced oxidative stress and intestinal toxicity in pigs. In this review, we systematically updated the latest research progress in plant polyphenols detoxifying DON-induced intestinal toxicity in swine. We also discussed the potential underlying mechanism of action of polyphenols as Nrf2 activators in protecting against DON-induced enterotoxicity of swine. The output of this update points out an emerging research direction, as polyphenols have great potential to be developed as feed additives for swine to counteract DON-induced oxidative stress and intestinal toxicity.

Tryptophan Alleviates Acute Heat Stress-Induced Impairment of Antioxidant Status and Mitochondrial Function in Broilers.

Heat stress has been considered as a critical risk factor for decreasing performance and causing oxidative stress in broilers. The tryptophan (TRP) derivative 5-hydroxytryptophan has been reported to protect membrane fluidity in broilers suffering from oxidative stress. Therefore, this experiment was conducted to investigate the effects of dietary TRP supplementation on antioxidant status and mitochondrial function-related genes expressions in broilers exposed to acute heat stress (34 ± 1°C, 24 h). Female Arbor Acres broilers (19-d-old, n = 180) were randomly assigned to 1 of 3 treatments. Broilers were fed a basal diet and in the thermoneutral conditions (TN, 23 ± 1°C) was considered as the TN group. Broilers were fed a basal diet and exposed to acute heat stress (HS, 34 ± 1°C) was regarded as the HS group. Broilers were fed a basal diet supplemented with 0.18% L-tryptophan and under HS conditions was treated as the HS + TRP groups. Heat stress led to increased malondialdehyde (MDA) concentration (P < 0.05), while it elevated catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and total antioxidant capacity activities (T-AOC) (P < 0.05) compared with the TN group. Nevertheless, compared with the HS group, TRP supplementation increased SOD activity (P < 0.05). The effects of acute heat stress were associated with increased mRNA abundance for redox-related genes (P < 0.05), and reduced mRNA levels for mitochondrial function-related genes (P < 0.05). Notably, the effects of acute heat stress on mitochondrial function-related genes expressions were reversed by TRP treatment. Collectively, dietary 0.18% TRP supplementation beneficially protects against acute heat stress-induced oxidation stress and mitochondrial dysfunction by regulating antioxidant states and increasing mitochondrial function-related genes expressions in broilers.

Effect of probiotic supplementation on the expression of tight junction proteins, innate immunity-associated genes, and microbiota composition of broilers subjected to cyclic heat stress.

This study investigated the effects of probiotic on intestinal innate immunity-associated gene expression and cecal microbiota in heat-stressed broilers. A total of 180 21-day-old male broilers were randomly assigned to three treatment groups with four replicates per group. The thermoneutral group (TN) (23 ± 1°C) received a basal diet, and another two heat-stressed groups (28-35-28°C for 12 h daily) were fed the basal diet (HS) or the basal diet supplemented with probiotic at a dose of 1.5 × 108 CFU/kg (HS_Pro) for 21 consecutive days. Compared with the TN group, the abundance of beneficial bacteria was decreased (p < 0.05) in the caecum of heat-stressed broilers. Heat stress downregulated (p < 0.05) the expression of Toll-like receptor (TLR)2 and upregulated (p < 0.05) the expressions of TLR5, TLR15, avian ß-defensin (AvBD)4, AvBD8, and AvBD14 in the ileum as compared with the TN group. Dietary supplementation of probiotic upregulated (p < 0.05) the occludin expression in the ileum, improved the microbiota balance in the caecum, and decreased (p < 0.05) the gene expressions of TLR5 and TLR15 in the ileum of heat-stressed broilers. Collectively, dietary probiotic supplementation could promote intestinal barrier function via improving gut microbiota community and regulating innate immunity-associated gene expressions in heat-stressed broilers.