Oleanolic acid improved intestinal immune function by activating and potentiating bile acids receptor signaling in E. coli-challenged piglets.

BACKGROUND: Infection with pathogenic bacteria during nonantibiotic breeding is one of the main causes of animal intestinal diseases. Oleanolic acid (OA) is a pentacyclic triterpene that is ubiquitous in plants. Our previous work demonstrated the protective effect of OA on intestinal health, but the underlying molecular mechanisms remain unclear. This study investigated whether dietary supplementation with OA can prevent diarrhea and intestinal immune dysregulation caused by enterotoxigenic Escherichia coli (ETEC) in piglets. The key molecular role of bile acid receptor signaling in this process has also been explored. RESULTS: Our results demonstrated that OA supplementation alleviated the disturbance of bile acid metabolism in ETEC-infected piglets (P < 0.05). OA supplementation stabilized the composition of the bile acid pool in piglets by regulating the enterohepatic circulation of bile acids and significantly increased the contents of UDCA and CDCA in the ileum and cecum (P < 0.05). This may also explain why OA can maintain the stability of the intestinal microbiota structure in ETEC-challenged piglets. In addition, as a natural ligand of bile acid receptors, OA can reduce the severity of intestinal inflammation and enhance the strength of intestinal epithelial cell antimicrobial programs through the bile acid receptors TGR5 and FXR (P < 0.05). Specifically, OA inhibited NF-κB-mediated intestinal inflammation by directly activating TGR5 and its downstream cAMP-PKA-CREB signaling pathway (P < 0.05). Furthermore, OA enhanced CDCA-mediated MEK-ERK signaling in intestinal epithelial cells by upregulating the expression of FXR (P < 0.05), thereby upregulating the expression of endogenous defense molecules in intestinal epithelial cells. CONCLUSIONS: In conclusion, our findings suggest that OA-mediated regulation of bile acid metabolism plays an important role in the innate immune response, which provides a new diet-based intervention for intestinal diseases caused by pathogenic bacterial infections in piglets.

Effects of sex on fat deposition through gut microbiota and short-chain fatty acids in weaned pigs.

Nitrogen pollution resulting from excessive feed consumption poses a significant challenge for modern swine production. Precision nutrition technology seems to be an effective way to solve this problem; therefore, understanding the law of pig body composition deposition is a prerequisite. This study investigated the sex effects on growth performance, body composition, nutrient deposition, gut microbiota, and short-chain fatty acids (SCFA) in weaned piglets. Eighty weaned pigs were randomly allocated to 2 treatments according to the sex of pigs. An individual pig was considered as a treatment replicate. Six body weights (BW 5, 7, 11, 15, 20, and 25 kg) were chosen as experimental points; for each point 10 piglets close to the average BW (5 males and 5 females) were slaughtered, and there was one growth phase between each 2 BW points. Results indicated that the males had higher average daily gain (ADG) and average daily feed intake (ADFI) compared to the females (P < 0.05) at growth phases 15 to 20 kg BW and 20 to 25 kg BW. Meanwhile, males at 20 kg BW had higher body fat content than females (P < 0.10). Males showed a higher body fat (P < 0.05) deposition rate at phase 15 to 20 kg BW (P < 0.05) than females. For pigs at 20 kg BW, the relative abundance of RuminococcaceaeUCG-005, Clostridium, Christensenellaceae_R-7_group, and Peptostreptococcaceae was significantly increased in males (P < 0.05) but that of Bifidobacterium was decreased (P < 0.05). At 25 kg BW, the relative abundance of Ruminococcaceae_NK4A214_group, Fibrobacter, RuminococcaceaeUCG-009, Ralstonia, Klebsiel, and Christensenellaceae_R-7_group in males was higher when compared with females (P < 0.05). In terms of SCFA, females exhibited higher concentrations of propionate compared to males (P < 0.05). The results of the current study indicated that sex influenced fat deposition through changes in the composition of gut microbiota and the content of SCFA, which has significant implications for the realization of precision nutrition in modern swine production.

Anti-Proteolytic Peptide R7I Protects the Intestinal Barrier and Alleviates Fatty Acid Malabsorption in Salmonella typhimurium-Infected Mice.

With a wide range of hosts, environmental adaptation, and antibiotic resistance, Salmonella typhimurium is one of the most common causes of food poisoning in the world. Infection with Salmonella typhimurium not only results in intestinal inflammation but also damages the intestinal barrier and interferes with the host's ability to absorb nutrients. It is imperative to find alternatives to antibiotics for eradicating bacteria, reducing intestinal damage, and reestablishing nutrient absorption, especially given that antibiotics are currently prohibited. This research aims to understand the protective role of anti-proteolytic peptide R7I on the gut in the setting of Salmonella typhimurium infection and its impact on nutritional absorption, maybe offering an alternative to antibiotics for bacterial killing. The findings demonstrated that R7I reduced the production of inflammatory factors, including IL-6, TNF-α, and L-1ß in the jejunum and decreased the expression of genes like TLR4 and NF-κB in the jejunum (p < 0.05). R7I enhanced antioxidant capacity and preserved the antioxidant/pro-oxidant balance in the jejunum (p < 0.05). R7I also normalized intestinal shape and restored tight junction protein expression. Fatty acid binding protein 2 (FABP2) and fatty acid transport protein 4 (FATP4) expression in the jejunum was restored by R7I. In addition, serum-free fatty acids and lipid metabolites were significantly higher in the R7I group than in the control group (p < 0.05). Overall, the anti-enzyme peptide R7I maintained the healthy state of the intestine and alleviated the abnormal fatty acid absorption caused by bacterial infection.

Branched-chain amino acid modulation of lipid metabolism, gluconeogenesis, and inflammation in a finishing pig model: targeting leucine and valine.

Branched-chain amino acids (BCAAs) play a regulatory role in adipogenesis and energy balance. Therefore, this study aimed to investigate the impact of BCAA supplements, especially leucine (Leu) and valine (Val) supplementation, on lipid metabolism and related disorders in a finishing pig model. The results demonstrated that Leu (1%) and Val decreased serum as well as hepatic lipid accumulation. Moreover, metabolomics and lipidomics analyses revealed that Leu and Val markedly downregulated the level of various lipid species in the liver. This outcome may be explained by Leu and Val promoting cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/hormone-sensitive triglyceride lipase (HSL) signaling pathways. Leu and Val altered the fatty acid composition in distinct adipose tissues and decreased the levels of inflammatory factors. Additionally, they significantly decreased back fat thickness, and the results of the fatty acid profiles demonstrated that Leu and Val significantly increased the levels of monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) while decreasing those of saturated fatty acids (SFAs), especially in back fat and abdominal fat. Besides, Leu and Val restored glucose homeostasis by suppressing gluconeogenesis through the serine/threonine protein kinase (AKT)/transcription factor forkhead box O1 (FOXO1) signaling pathway in the liver and back fat. In summary, these results suggest that Leu and Val may serve as key regulators for modulating lipid metabolism and steatosis.

Aquaporin: targets for dietary nutrients to regulate intestinal health.

Aquaporins (AQP) are a class of water channel membrane proteins that are widely expressed in the gut. The biological functions of aquaporins, which regulate the absorption and secretion of water molecules and small solutes, maintain the stable state of the intestine, regulate cell proliferation and migration, participate in the process of intestinal inflammation, and mediate tumorigenesis, demonstrate the physiological significance of these channels in intestinal health. The pathology of many intestinal diseases is associated with changes in the location and expression of aquaporins, such as intestinal infection, which can change the expression and distribution of AQPs in intestinal tissues/cells by affecting cytokines and chemokines. This can lead to various intestinal diseases such as diarrhoea, which also suggests the importance of aquaporins in the prevention and treatment of intestinal diseases. This review summarizes the relationship between aquaporins and intestinal physiology and diseases and focuses on drugs (such as plant extracts) or diets that can regulate intestinal health by regulating aquaporins. It provides a basis for establishing aquaporins as biomarkers and therapeutic targets for intestinal health.

Tryptophan Promotes Intestinal Immune Defense through Calcium-Sensing Receptor (CaSR)-Dependent Metabolic Pathways.

The gastrointestinal tract forms a robust line of defense against invading pathogens through the production of endogenous antimicrobial peptides (AMPs), which are crucial molecules of the innate defense system. Tryptophan could modulate intestinal immunity through promoting the expression of AMPs. However, the precise mechanism needs to be further clarified. In this study, we show that treatment with tryptophan for 24 h triggers (p < 0.05) the expression of porcine ß-defensin (pBD) 1 (62.67 ± 3.10 pg/mL) and pBD2 (74.41 ± 1.33 pg/mL) in the porcine intestinal epithelial cells (IPEC-J2) though calcium-sensing receptor (CaSR)-tryptophan metabolic pathways. Meanwhile, tryptophan alleviates (p < 0.05) intestinal inflammation induced by lipopolysaccharide (LPS) through induction of the defensins and activation of the CaSR-AMP-activated protein kinase (AMPK) pathways in vitro and in vivo. Moreover, the activation of CaSR induces the expression of defensins and decreases the levels of IL-1ß (75.26 ± 2.74 pg/mL) and TNF-α (449.8 ± 23.31 pg/mL) induced by LPS (p < 0.05). Importantly, tryptophan maintains kynurenine homeostasis through the activation of CaSR during the inflammatory response. To that end, the work identifies a regulatory circuit between CaSR signaling and tryptophan metabolic pathways involved in the tryptophan-trigged AMP expression, which contributes to improving intestinal immune defense.

Deoxynivalenol exposure induces liver damage in mice: Inflammation and immune responses, oxidative stress, and protective effects of Lactobacillus rhamnosus GG.

Deoxynivalenol (DON), one of the most common environmental pollutants, substantially affects human and animal health. Much attention has been paid to the ability of probiotics to modulate inflammation and immune responses. In this work, the toxic effects of DON on the liver and the protective effects of Lactobacillus rhamnosus GG (LGG) were investigated. We treated mice with oral gavage of DON (2.4 mg/kg bw/day), LGG (1 × 109 CFU/mouse/day) or both for 28 days. The results showed that DON triggered liver inflammation, reflected by pathological changes and liver function damage but LGG oral administration significantly attenuated these changes. Notably, DON treatment activated the TLR4/NF-κB signaling pathway which contribute to produce inflammatory cytokines, but oral administration of LGG inhibited all the effects of DON. DON treatment can also induce oxidative stress and activate Keap1-Nrf2 signaling pathway, leading to the activation of Nrf2 and the downstream genes, while LGG treatment can improve the antioxidant capacity of liver and protected mice from DON injury. In conclusion, LGG was able to negate the detrimental effects of DON on the liver and may contribute as a potential dietary intervention strategy to reduce mycotoxicity.

Oleanolic Acid Targets the Gut-Liver Axis to Alleviate Metabolic Disorders and Hepatic Steatosis.

This study investigated the effects of oleanolic acid (OA) on hepatic lipid metabolism and gut-liver axis homeostasis in an obesity-related non-alcoholic fatty liver disease (NAFLD) nutritional animal model and explored possible molecular mechanisms behind its effects. The results revealed that OA ameliorated the development of metabolic disorders, insulin resistance, and hepatic steatosis in obese rats. Meanwhile, OA restored high-fat-diet (HFD)-induced intestinal barrier dysfunction and endotoxin-mediated induction of toll-like-receptor-4-related pathways, subsequently inhibiting endotoxemia and systemic inflammation and balancing the homeostasis of the gut-liver axis. OA also reshaped the composition of the gut microbiota of HFD-fed rats by reducing the Firmicutes/Bacteroidetes ratio and increasing the abundance of butyrate-producing bacteria. Our results support the applicability of OA as a treatment for obesity-related NAFLD through its anti-inflammatory, antioxidant, and prebiotic integration responses mediated by the gut-liver axis.

Plant Polyphenols: Potential Antidotes for Lead Exposure.

Lead is one of the most common heavy metal elements and has high biological toxicity. Long-term lead exposure will induce the contamination of animal feed, water, and food, which can cause chronic lead poisoning including nephrotoxicity, hepatotoxicity, neurotoxicity, and reproductive toxicity in humans and animals. In the past few decades, lead has caused widespread concern because of its significant threat to health. A large number of in vitro and animal experiments have shown that oxidative stress plays a key role in lead toxicity, and endoplasmic reticulum (ER) stress and the mitochondrial apoptosis pathway can also be induced by lead toxicity. Therefore, plant polyphenols have attracted attention, with their advantages of being natural antioxidants and having low toxicity. Plant polyphenols can resist lead toxicity by chelating lead with their special chemical molecular structure. In addition, scavenging active oxygen and improving the level of antioxidant enzymes, anti-inflammatory, and anti-apoptosis are also the key to relieving lead poisoning by plant polyphenols. Various plant polyphenols have been suggested to be useful in alleviating lead toxicity in animals and humans and are believed to have good application prospects.

Sodium houttuyfonate enhances the intestinal barrier and attenuates inflammation induced by Salmonella typhimurium through the NF-κB pathway in mice.

Salmonella typhimurium (ST), as an aggressive bacterium, mainly causes intestinal inflammation and diarrhea. Sodium houttuyfonate (SH) is a derivative of houttuynin in the active oil of Houttuynia cordata, which is stable in nature and has anti-inflammatory activity. In this study, we used BALB/c mice infected with ST as experimental subjects and aimed to study the regulatory effect of SH on the intestinal tract and to explain its anti-inflammatory mechanism. Compared with the ST group, SH treatment improved the morphology of jejunum mucosa and alleviated the pathological damage to colon tissue. In addition, SH protected the intestinal barrier by regulating the localization and distribution of tight junction proteins. Meanwhile, SH significantly decreased the production of pro-inflammatory cytokines (TNF-α, IL-1ß, IL-6) and inflammation-related enzymes (iNOS, COX-2). Moreover, further western blot results suggested that SH inhibited the expression of p-IκBα and p-p65 in intestinal tissues. These results demonstrated that SH maintained the intestinal barrier and attenuated the production of intestinal proinflammatory cytokines by regulating the NF-κB signaling pathway, thereby providing protection for the intestine.

Hybridization with Insect Cecropin A (1-8) Improve the Stability and Selectivity of Naturally Occurring Peptides.

Antimicrobial peptides (AMPs) offer great hope and a promising opportunity to overcome the rapid development of drug-resistant pathogenic microbes. However, AMPs often lack the stability required for a successful systemic drug. Hybridizing different AMPs is a simple and effective strategy to obtain novel peptides. N-terminal fragment of cecropin A (CA (1-8)) is often used to hybridize with other AMPs to reduce cytotoxicity. However, hybridizing with CA (1-8) in improving the stability of AMPs is not clear. Therefore, a series of peptides were designed by combining with CA (1-8) and their antibacterial activity and stability in the presence of salts and human serum were evaluated. The resultant α-helical hybrid peptide CA-FO composed of CA (1-8) and the most potent region of Fowlicidin-2 (FO (1-15)) exhibited excellent antibacterial activity (2-8 µM) and cell selectivity toward bacterial over mammalian cells. Moreover, CA-FO still retained vigorous antimicrobial activity in the presence of human serum and salts at physiological concentrations. CA-FO exhibited effective antibacterial activity by increasing membrane permeability and damaging membrane integrity. In conclusion, these results indicated the success of hybridization in designing and optimizing AMPs with improved stability and selectivity and the peptide CA-FO can be further evaluated as peptide-therapy to treat bacterial infections.

Oleanolic acid enhances tight junctions and ameliorates inflammation in Salmonella typhimurium-induced diarrhea in mice via the TLR4/NF-κB and MAPK pathway.

Salmonella typhimurium (S.T) is a common cause of acute, self-limiting food-borne diarrhea with severe intestinal inflammation and intestinal barrier damage. Oleanolic acid (OA), isolated from almost 2000 plant species, has been shown to have anti-inflammatory roles. The purpose of this study was to investigate the potential protective effects of OA on S.T-induced diarrhea and enteritis and to elucidate its anti-inflammatory mechanisms. A total of eighty BALB/c mice (4-week-old) were randomly divided into the control group (no S.T, no OA), the S.T group (S.T only), the S.T + OA group (S.T plus 100 mg kg-1 OA) and the OA group (100 mg kg-1 OA only). Compared with the S.T group, OA administration significantly reduced clinical symptoms and weight loss, and the severity of diarrhea and intestinal structural damage was significantly alleviated, which was confirmed by a decrease in the diarrhea index (DI) and jejunal histological damage. In addition, in the infected jejunum, OA maintained the expression and localization of occludin, claudin-1 and ZO-1 to protect the jejunal barrier, thereby maintaining the integrity of the gut barrier. Finally, OA treatment not only reduced the levels of COX-2 and iNOS but also inhibited the secretion of pro-inflammatory cytokines, such as IL-1ß, IL-6 and TNF-α. Furthermore, western blotting results showed that OA treatment significantly inhibited IκB phosphorylation and degradation in intestinal tissues and the nuclear translocation of p65, and OA also decreased the level of TLR4 and the activation of the MAPK pathway. To summarise, OA can maintain the intestinal tight junction barrier and prevent diarrhea caused by S.T. as well as reduce intestinal inflammation through the NF-κB and MAPK signaling pathways.

Effects of dietary γ-aminobutyric acid supplementation on antioxidant status, blood hormones and meat quality in growing-finishing pigs undergoing transport stress.

γ-Aminobutyric acid (GABA) is a natural nonprotein amino acid distributed in animals, plants and microbes. GABA is an inhibiting neurotransmitter which takes great effect in mammalian central nervous system. We carried out the research to study the influence of GABA on blood hormone concentrations, antioxidant status and meat quality in fattening pigs after transportation. The 72 pigs with a starting weight of approximately 32.67 ± 0.62 kg were randomly allocated to 2 groups based on dietary treatments, containing 6 replicates with 6 pigs in each. The pigs were fed dietary supplementation of GABA (0 or 30 mg/kg of diets) for 74 days. Twelve pigs were randomly selected from each group and assigned to the either 1 hr of transport (T group) or no transport (N group), resulting in two-factor factorial design. Compared to the control, GABA supplementation increased average daily gain (ADG) (p < .01) and decreased feed-gain ratio (F/G) (p < .05). The pH45 min was lower and drip loss was greater in the longissimus muscles (LM) of post-slaughter of transported pigs (p < .05). The pH45 min of 0/T group (group with 0 mg/kg GABA and transport) was significantly lower than the pH45 min of the 30/T group (diet × transport; p < .05). GABA supplementation significantly increased serum glutathione peroxidase (GSH-Px) concentration (p < .05) before transportation. Following transport, pigs fed GABA had decreased concentrations of serum malonaldehyde (MDA), adrenal cortical hormone and cortisol (p < .05). The results indicate that feeding GABA significantly increased the growth performance of growing-finishing pigs. The transportation model negatively impacted meat quality, antioxidant indexes and hormone parameters, but dietary supplementation of GABA could suppress the rise of drip loss of LM, ACTH and COR and suppress the drop of pH45 min of LM after transportation stress in growing-finishing pigs. Feeding GABA alleviated transportation stress in pigs.

Effect of fermented blood cells on growth performance and intestinal characteristics of weaned piglets.

The increase in feed costs has led feeder to replace protein source. Blood meal can be used in piglet diets instead of fish meal (FM). The objective of this study was to investigate the effect of fermented blood cells (FBCs) on the growth performance and intestinal health of weaned piglets. One hundred eighty 28-day-old piglets were assigned and were divided into 4 groups (9 L per groups and 5 pigs per litters) randomly. The piglets were fed one of four experimental diets, fish meal, blood cells (BCs), liquid-state fermented blood cells (LFBCs) or solid-state fermented blood cells (SFBCs) respectively. The dietary with LFBCs and SFBCs increased the average daily gain and feed intake (ADFI) and average daily gain (ADG) (p < .05). In duodenum, LFBC group increased the villous height (p < .05). The SFBC and LFBC group significantly increased the villous height (p < .05) in the jejunum. Fermented blood cells exhibit a positive regulatory function on the intestinal tract and modulate intestinal microflora. Compared with the fish meal group, the CAT, GSH-PX and SOD activity, and MDA level was no significant differences in jejunum and plasma of weaned piglets (p > .05). LFBCs and SFBCs significantly increased the bifidobacteria and lactobacillus number in the caecum (p < .05). Dietary LFBCs increased the expression of ZO-1 mRNA in the jejunal of weaned piglets (p < .05). In conclusion, dietary with fermented blood cells in weaned piglets had improved growth performance and intestinal health of weaned piglets.

Ethyl pyruvate inhibits LPS induced IPEC-J2 inflammation and apoptosis through p38 and ERK1/2 pathways.

The endotoxin of Gram-negative bacteria threatens the intestinal health of livestock. Ethyl pyruvate (EP) has been shown to regulate intestinal immunity and protect against cell and tissue damage. In this study, it was first verified that EP could reduce the secretion of IL-8, TNF-α, IL-6 and IL-1ß in LPS-induced IPEC-J2 cells. Then, we used RNA sequencing (RNA-seq) to analyze the differentially expressed genes (DEGs) of inflammatory factors induced by LPS in IPEC-J2 cells. It was found that LPS induced the upregulation of 377 genes and the downregulation of 477 genes compared to Vehicle; LPS+EP induced the upregulation of 258 genes and the downregulation of 240 genes compared to Vehicle; and LPS+EP induced the upregulation of 373 genes and the downregulation of 188 genes compared to LPS (fold change > 1.5 and FDR < 0.01). Their enrichment pathways included the MAPK signaling pathway, PI3K-Akt signaling pathway, Toll-like receptor signaling pathway, and other pathways. Furthermore, the mRNA level of cytokines associated with inflammation and apoptosis enriched in the MAPK pathway was verified by qRT-PCR. Western blots and immunofluorescence revealed that EP significantly inhibited phosphorylated p38 and phosphorylated-ERK1/2 protein expression levels (P < 0.05). The apoptosis due to LPS reduced by EP was significantly inhibited, as shown by Annexin V-FITC/PI staining. According to the results, EP inhibited the expression of IL-8, TNF-α, IL-6 and IL-1ß as well as apoptosis by inhibiting the phosphorylation of p38 and ERK1/2 in LPS-induced IPEC-J2 cells.

Bioactivity and Bactericidal Mechanism of Histidine-Rich ß-Hairpin Peptide Against Gram-Negative Bacteria.

Antibacterial peptides (APMs) are a new type of antibacterial substance. The relationship between their structure and function remains indistinct; in particular, there is a lack of a definitive and fixed template for designing new antimicrobial peptides. Previous studies have shown that porcine Protegrin-1 (PG-1) exhibits considerable antimicrobial activity and cytotoxicity. In this study, to reduce cytotoxicity and increase cell selectivity, we designed histidine-rich peptides based on the sequence template RR(XY)2XDPGX(YX)2RR-NH2, where X represents I, W, V, and F. The results showed that the peptides form more ß-hairpin structures in a lipid-rich environment that mimics cell membranes. Among them, the antimicrobial peptide HV2 showed strong antibacterial activity against Gram-negative strains and almost no toxicity to normal cells. The results of our analysis of its antibacterial mechanism showed that peptide HV2 acts on the bacterial cell membrane to increase its permeability, resulting in cell membrane disruption and death. Furthermore, peptide HV2 inhibited bacterial movement in a concentration-dependent manner and had a more robust anti-inflammatory effect by inhibiting the production of TNF-α. In summary, peptide HV2 exhibits high bactericidal activity and cell selectivity, making it a promising candidate for future use as an antibiotic.

Astragalus polysaccharides attenuated inflammation and balanced the gut microflora in mice challenged with Salmonella typhimurium.

Salmonella typhimurium (S. t.) is one of the main pathogens that causes acute gastroenteritis. To evaluate the anti-inflammatory mechanism of Astragalus polysaccharide (APS) in vivo and its influence on the intestinal flora, BALB/c mice were infected with S. t. to establish a model of diarrhea. The disease activity index (DAI) scores showed that APS attenuated S. t.-induced weight loss and diarrhea in mice. APS significantly reduced the index of the liver and spleen as well as the ALT and AST levels in serum (P < 0.05). Hematoxylin and eosin (H&E) results indicated that APS significantly increased jejunum villus height and crypt depth and reduced the infiltration of inflammatory cells (P < 0.05). Additionally, APS increased the tight junction (TJ) proteins expression levels of ZO-1, Occludin and Claudin-1 in the jejunum. The results of 16S rDNA showed that APS significantly increased the number of Lactobacillus and Bifidobacterium spp. to normal levels (compared with the control group). In addition, APS significantly decreased the mRNA expression levels of the proinflammatory cytokines TNF-α, IL-1ß, IL-6 and IL-17 in the jejunum (P < 0.01) as well as the proteins expression levels of COX-2 and iNOS (P < 0.05). Western blot confirmed that prefeeding with APS inhibited S. t.-induced expression of TLR4 and MyD88 in the jejunum and further inhibited nuclear factor-κB (NF-κB) activation, including the nuclear translocation of the p65 NF-κB subunit and the phosphorylation and degradation of IκB-α. This was the key to APS inhibition of the production of inflammatory factors and inflammatory mediators in the jejunum.

Effects of dietary resveratrol supplementation during gestation and lactation of sows on milk composition of sows and fat metabolism of sucking piglets.

The purpose of this article was to investigate the effects of dietary resveratrol supplementation during gestation and lactation of sows on the milk composition of sows and the fat metabolism of sucking piglets. Forty sows were allotted to two experimental treatment groups that included the following: (a) control sows (CON treatment, n = 20) fed with a corn-soybean meal control diet and (b) treatment sows (RES treatment, n = 20) fed with a control diet with addition of 300 mg/kg resveratrol. The results showed that the content of lactose in the colostrum was increased (p < 0.05) and the content of fat in 21-day milk was increased (p < 0.05) by dietary resveratrol supplementation. In the RES treatment group, the concentrations of high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), lipase activity and insulin (INS) in plasma of sucking piglets were increased (p < 0.05). In the adipose tissue, the enzyme activities of hormone-sensitive lipase (HSL), acetyl-CoA carboxylase (ACC) and lipoprotein lipase (LPL) increased significantly by RES treatment (p < 0.05), and the mRNA levels of acetyl coenzyme A-alpha (ACCα), LPL, fatty acid transport protein (FATP1) and CCAAT-enhancer-binding protein gene (C/EBPα) were higher in the RES treatment group (p < 0.05). In conclusion, resveratrol supplementation on gestational and lactating sows improved the content of lactose in the colostrum and the content of fat in milk at day 21 of lactation. In addition, resveratrol supplementation on sows increased HDL and LDL in the plasma of piglets. In piglet adipose tissue, the enzyme activity and mRNA level related to lipolysis, fatty acid uptake from circulating triacylglycerols and lipogenesis are partially improved by resveratrol supplementation on sows. These aspects affect fat metabolism in piglets.

Modified halloysite nanotubes reduce the toxic effects of zearalenone in gestating sows on growth and muscle development of their offsprings.

BACKGROUND: Zearalenone (ZEN) is an estrogenic mycotoxin that is primarily produced by Fusarium fungi and has been proven to affect the reproductive capacity of many species to varying degrees. The present experiment was designed to study the maternal persistent effects of zearalenone toxicity in gestating sows on growth and muscle development of their offsprings, and the alleviation of zearalenone toxicity by modified halloysite nanotubes (MHNTs). METHODS: Eighteen sows were fed with one of three dietary treatments that included the following: (1) a control diet, (2) a contaminated grain diet (with 50 % moldy corn, 2.77 mg/kg ZEN), and (3) a contaminated grain diet (with 50 % moldy corn, 2.76 mg/kg ZEN) + 1 % MHNTs. Each sow was exclusively fed its experimental diets from 35 to 70 d of gestation at a total of 2 kg daily. Muscle samples were collected from six piglets per treatment at birth, weaning and finishing. RESULTS: The results showed that feeding the sows with the ZEN-contaminated diets from 35 to 70 d of gestation decreased the ADG, ADFI and G:F of their offsprings (P < 0.05). The muscle fiber numbers in the newborn, weaning and growing-finishing pigs and the muscle fiber diameters at birth and weaning were also decreased by maternal ZEN exposure (P < 0.05). The expressions of IGF-I, IGF-II, Myf-5 and Mstn at birth and IGF-II, Pax7, Myf-5 and MyoD1 at weaning were altered by feeding gestating sows with ZEN-contaminated diets (P < 0.05). The MHNTs reduced most of the ZEN-induced toxic effects: the ADG and ADFI on growth performance, the muscle fiber numbers at weaning and finishing and the muscle fiber diameters at weaning (P < 0.05). The expression levels of IGF-II and Mstn in newborn piglets and IGF-II and Myf-5 in weaning piglets were also prevented by adding 1 % MHNTs (P < 0.05). CONCLUSIONS: The present study demonstrated that the offsprings of sows fed with ZEN-contaminated diets from 35 to 70 day of gestation exhibited weakening on growth performance, physiological changes in their muscle fibers and alterations of mRNA expression in their muscle tissues, and also indicated that MHNTs prevented most of the ZEN-induced weakening in the muscle tissues.