Background The benefits of combining benzoic acid and essential oils (BAO) to mitigate intestinal impairment during the weaning process have been well established, while the detailed underlying mechanism has not been fully elucidated. Previous research has primarily focused on the reparative effects of BAO on intestinal injury, while neglecting its potential in enhancing intestinal stress resistance. Methods In this study, we investigated the pre-protective effect of BAO against LPS-induced stress using a modified experimental procedure. Piglets were pre-supplemented with BAO for 14 d, followed by a challenge with LPS or saline to collect blood and intestinal samples. Results Our findings demonstrated that BAO supplementation led to significant improvements in piglets' final weight, average daily gain, and feed intake/body gain ratio. Additionally, BAO supplementation positively influenced the composition of intestinal microbiota, increasing beneficial Actinobacteriota and Alloprevotella while reducing harmful Desulfobacterota, Prevotella and Oscillospira . Furthermore, BAO supplementation effectively mitigated oxidative disturbances and inflammatory responses induced by acute LPS challenge. This was evidenced by elevated levels of T-AOC, SOD, and GSH, as well as decreased levels of MDA, TNF-α, and IL-6 in the plasma. Moreover, piglets subjected to LPS challenge and pre-supplemented with BAO exhibited significant improvements in intestinal morphological structure and enhanced integrity, as indicated by restored expression levels of Occludin and Claudin-1 compared to the non-supplemented counterparts. Further analysis revealed that BAO supplementation enhanced the jejunal antioxidative capacity by increasing GSH-Px levels and decreasing MDA levels under the LPS challenge and stimulated the activation of the Nrf2 signaling pathway. Additionally, the reduction of TLR4/NF-κB/MAPK signaling pathways activation and proinflammatory factor were also observed in the jejunal of those piglets fed with BAO. Conclusions In summary, our study demonstrates that pre-supplementation of BAO enhances the anti-stress capacity of weaned piglets by improving intestinal microbiota composition, reinforcing the intestinal barrier, and enhancing antioxidative and anti-inflammatory capabilities. These effects are closely associated with the activation of Nrf2 and TLR4/NF-κB/MAPK signaling pathways.

The exacerbation of the greenhouse effect has made heat stress (HS) an important risk factor for the occurrence of intrauterine growth restriction (IUGR). The experiment aims to uncover the effects of maternal HS on IUGR and its mechanisms. The results showed that HS leads to decreased maternal and fetal birth weights, accompanied by increased serum oxidative stress and cortisol levels. Moreover, HS inflicted significant damage to both the intestinal and placental barriers, altering maternal gut microbiota and increasing intestinal LPS levels. As a result, LPS levels increased in maternal serum, placenta, and fetus. Furthermore, HS damaged the intestinal structure, intensifying inflammation and disrupting the redox balance. The placenta exposed to HS exhibited changes in the placental structure along with disrupted angiogenesis and decreased levels of nutritional transporters. Additionally, the leakage of LPS triggered placental JNK and ERK phosphorylation, ultimately inducing severe placental inflammation and oxidative stress. This study suggests that LPS translocation from the maternal intestine to the fetus, due to a disrupted gut microbiota balance and compromised intestinal and placental barrier integrity, may be the primary cause of HS-induced IUGR. Furthermore, increased LPS leakage leads to placental inflammation, redox imbalance, and impaired nutrient transport, further restricting fetal growth.

Comprehensive studies have been conducted to compare the effect of organic and inorganic selenium previously, but there is still limited knowledge about the difference between organic selenium (Se) from varied sources despite the widely use of organic Se in both animal and human being nutrient additives. In the present study, we systemically compared the effect of two different types of organic Se including selenium yeast (SeY) and selenium methionine (Sel-Met) on cell viability, selenoprotein transcriptome, and antioxidant status in porcine mammary epithelial cells (PMECs) and the results indicated that appropriate addition of SeY and Sel-Met both significantly promoted cell viability and up-regulated the mRNA expression of most selenopreoteins including DIOs, GPXs, and TrxRs family et al. (P < 0.05). Besides, two different sources of Se supplementation both greatly improved redox status with higher levels of T-AOC, SOD, and CAT (P < 0.05), while less content of MDA (P < 0.05), and reduced protein expression of cleaved-caspase-3 (P < 0.05) to mitigate cell apoptosis. Furthermore, the key proteins related to p38/JNK pathway including p38, p-p38, JNK, and p-JNK were apparently reduced in the groups with both of SeY and Sel-Met (P < 0.05). Interestingly we found that the changes induced by SeY supplementation in cell viability, selenoprotein transcriptome, antioxidative capacity, and anti-apoptosis were comprehensively greater compared with same levels addition of Sel-Met in PEMCs (P < 0.05). In conclusion, both SeY and Sel-Met promoted cell viability and attenuated cell apoptosis by regulating the selenoprotein expression and antioxidative capacity via p38/JNK signaling pathway in PMEC, but SeY has more efficient benefits than that of Sel-Met.

本试验采用猪乳腺上皮细胞作为体外模型探讨亮氨酸对乳成分合成的影响及其分子机制.分别用0(对照组)、1、5和10 mmol/L的亮氨酸处理猪乳腺上皮细胞24和48 h后,检测细胞活力,分析乳蛋白、氨基酸转运载体、葡萄糖转运载体及脂肪酸转运载体的基因表达情况,并进一步检测哺乳动物雷帕霉素靶蛋白(mTOR)信号通路中关键蛋白mTOR和核糖体蛋白S6激酶1(S6K1)的表达和磷酸化情况以期探索体外亮氨酸调控乳成分合成的机制.结果显示:不同浓度亮氨酸处理48 h后细胞活力均较对照组显著提高(P<0.05),且以亮氨酸浓度为1 mmol/L时细胞活力最高.与对照组相比,1 mmol/L组的αs2-酪蛋白(CSN1S2)和κ-酪蛋白(CSN3)mRNA相对表达量显著提高(P<0.05),5 mmol/L组的CSN1S2 mRNA相对表达量显著提高(P<0.05).与对照组相比,氨基酸转运体溶质载体家族1成员4(SLC1A4)、溶质载体家族7成员11(SLC7A11)、溶质载体家族7成员5(LAT1)、溶质载体家族7成员7(SLC7A7)和脂肪酸转运蛋白1(FATP1)的mRNA相对表达量在1 mmol/L组、5 mmol/L组、10 mmol/L组中均显著升高(P<0.05);溶质载体家族38成员1(SNAT1)、溶质载体家族7成员2(SLC7A2)、脂肪酸转运蛋白2(FATP2)、脂肪酸结合蛋白7(FABP7)的mRNA相对表达量在1 mmol/L组、5 mmol/L组中显著升高(P<0.05);溶质载体家族1成员5(SLC1A5)的mRNA相对表达量在1 mmol/L组、10 mmol/L组中显著升高(P<0.05);溶质载体家族3成员2(4F2hc)、溶质载体家族3成员1(rBAT)和脂肪酸移位酶(CD36)的mRNA相对表达量在5 mmol/L组、10 mmol/L组中显著升高(P<0.05);此外,1 mmol/L亮氨酸处理还显著提高了FATP1、脂肪酸结合蛋白3(FABP3)、脂肪酸结合蛋白5(FABP5)和酰基辅酶A结合蛋白(ACBP)的mRNA相对表达量(P<0.05);而葡萄糖转运体8(GLUT8)的mRNA相对表达量在5 mmol/L组和10 mmol/L组中均显著降低(P>0.05).与对照组相比,1 mmol/L亮氨酸处理显著提高了S6K1的磷酸化水平(P<0.05),但各浓度亮氨酸组mTOR的磷酸化水平无显著变化(P>0.05).综上可知,在培养基中添加亮氨酸可提高猪乳腺上皮细胞活力,促进乳蛋白、氨基酸转运载体和脂肪酸转运载体基因的表达.

Artemisia annua L. (A. annua) contains artemisinin, which attracts attention on account of its anti-inflammatory and anti-oxidant effects. Increased intestinal inflammation, oxidative stress, and hypoimmunity commonly occur in neonatal and early-weaning piglets. Abundant evidence suggests that maternal nutritional interventions during pregnancy modify the offspring's long-term gut development. The present study was conducted to investigate the effects of maternal A. annua extract (AAE) supplementation on the offspring's intestinal inflammation and redox status. A total of 90 pregnant sows were assigned randomly and equally into the control (CON) group (fed with a basal diet) and the 0.1% (AAE) group (basal diet with 1.0 g kg-1 AAE) during late gestation and lactation. The results showed that 0.1% AAE supplementation significantly decreased the contents and relative mRNA expressions of interleukin (IL)-1β, IL-6, and IL-12, and tumor necrosis factor-α in the small intestine of the newborn and weaned piglets (offspring) (P < 0.05). There were higher activities of total antioxidant capacity and total superoxide dismutase, whereas a lower concentration of malondialdehyde in the small instestine of offspring in the 0.1% AAE group than that in the CON group (P < 0.05). Furthermore, the 0.1% AAE group decreased the mRNA and protein expressions of Toll-like receptor 4 (TLR4) and inhibited the activation of TLR4-mediated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways (P < 0.05). The mRNA expression of peroxisome proliferator activated receptor γ (PPARγ), porcine beta-defensin (PBD)-1, PBD-2, PBD-3, mucin (MUC)-1, MUC-2 and MUC-4 was significantly enhanced in the small intestine of both neonatal and weanling piglets (P < 0.05). Together, these results showed that maternal 0.1% AAE supplementation improved the redox status and attenuated the neonatal and early-weaning associated inflammatory response in the offspring's small intestine, possibly by suppressing the activation of the TLR4/NF-κB and MAPK inflammatory pathways, and stimulated expressions of beta-defensins, mucins, and PPARγ to promote inflammation resolution and innate immunity response.

In a previously published study we reported that sow dietary leucine supplementation during late pregnancy significantly improved newborn piglet birth weight by stimulating protein synthesis in the longissimus dorsi muscle. However, there is still limited knowledge as to whether leucine can exert its effects on the placenta, one of the most important temporal organs during pregnancy, to promote maternal-fetal nutrient supply and thus contribute to fetal intrauterine development. Therefore, we tested this hypothesis in the present study. In total, 150 sows at day 90 of gestation were divided into three groups and fed with either a control diet (CON), CON + 0.4% Leu or CON + 0.8% Leu, respectively, until parturition. Placental metabolomics, full spectrum amino acids and nutrient transporters were systematically analyzed after sample collection. The results indicated that Leu supplementation led to an altered placental metabolism with an increased number of metabolites related to glycolysis and the oxidation of fatty acids, as well as elevated levels of amino acid accumulation in the placenta. In addition, nutrient transporters of amino acids, glucose and fatty acids in the placenta were globally up-regulated and several enzymes related to energy metabolism, including hexokinase, succinate dehydrogenase, lactated hydrogenase, glycogen phosphorylase and hydroxyacyl-CoA-dehydrogenase, were also significantly increased with no change observed in the antioxidative status of those groups with Leu supplementation. Furthermore, the phosphorylation of PI3K, Akt, and mTOR was enhanced in the placenta of sows undergoing Leu treatment. Collectively, we concluded that supplementing the diets of sows with Leu during late gestation globally altered placental metabolism and promoted maternal-fetus nutrient transport (amino acids, glucose, and fatty acids) via modulation of the PI3K/Akt/mTOR signaling pathway.

BACKGROUND:Intrauterine growth restriction (IUGR) is a major inducer of higher morbidity and mortality in the pig industry and catch-up growth (CUG) before weanling could significantly restore this negative influence. But there was limited knowledge about the underlying mechanism of CUG occurrence.METHODS:Eighty litters of newborn piglets were divided into normal birth weight (NBW) and IUGR groups according to birth weight. At 26 d, those piglets with IUGR but over average body weight of eighty litters of weaned piglets were considered as CUG, and the piglets with IUGR still below average body weight were considered as NCUG. This study was conducted to systemically compare the intestinal difference among NBW, CUG and NCUG weaned piglets considering the crucial role of the intestine for piglet growth.RESULTS:The results indicated that the mRNA expression of nutrients (amino acids, glucose, and fatty acids) transporters, and mitochondrial electron transport chain (ETC) I were upregulated in CUG piglets' gut with improved morphology compared with those NCUG, as well as the ratio of P-AMPK/AMPK protein expression which is the indicator of energy metabolism. Meanwhile, CUG piglet's gut showed higher antioxidative capacity with increased SOD and GSH-Px activity, decreased MDA levels, as well as higher mRNA expressions of Nrf2, Keap1, SOD, and GSH-Px. Furthermore, inflammatory parameters including TNF-α, IL-1β, IL-6, and IL-12 factors, and the activation of MAPK and NF-κB signaling pathways were significantly elevated in the NCUG intestine, while the protein expression of ZO-1, Occludin and Claudin-1 was reduced. The alpha diversity of fecal microbiota was higher in CUG piglets in contrast with NCUG piglets, and the increased beneficial bacteria and decreased pathogenic bacteria was also observed in CUG piglets.CONCLUSIONS:CUG piglet's intestine showed comprehensive restoration including higher nutrients transport, energy metabolism, antioxidant capacity, and intestinal physical barrier, while lower oxidative stress, inflammatory response, and pathogenic microbiota.

Frequent occurrence of intrauterine growth restriction (IUGR) causes huge economic losses in the pig industry. Accelerated catch-up growth (CUG) in the early stage of life could restore multiple adverse outcomes of IUGR offspring; however, there is little knowledge about this beneficial phenomenon. We previously found that nutrient absorption related to intestinal function was globally promoted in CUG-IUGR piglets before weaning, which might be the dominant reason for CUG, but what this alteration could lead to in subsequent liver metabolism is still unknown. Firstly, a Normal, CUG, and non-catch-up growth (NCUG) piglet model before weaning was established by dividing eighty litters of newborn piglets into normal birth weight (NBW) and IUGR groups according to birth weight, and those piglets with IUGR but above-average weanling body weight were considered CUG, and the piglets with IUGR still below average body weight were considered NCUG at weaning day (d 26). Liver samples were collected and then systematically compared in glycolipid metabolism, mitochondrial function, antioxidant status, and inflammatory status among these three different growth models. Enhanced hepatic uptake of fatty acids, diminished de novo synthesis of fatty acids, and increased oxidation of fatty acids were observed in CUG livers compared to Normal and NCUG. In contrast, the NCUG liver showed enhanced glucose uptake and gluconeogenesis compared to Normal and CUG. We also observed deteriorating hepatic vacuolation in NCUG piglets, while increasing hepatic lipid deposition in CUG piglets. Besides, the expression of genes related to mitochondrial energy metabolism and biogenesis was reduced in CUG piglets and the phosphorylation level of AMPK was significantly higher compared to Normal (p < 0.05). Moreover, NCUG liver showed decreased T-AOC (p < 0.01) and GSH-PX (p < 0.05), increased MDA concentrations (p < 0.01), upregulated phosphorylation levels of ERK and NF-κB (p < 0.05), and elevated pro-inflammatory factors IL-1β, IL-6 and TNF-α (p < 0.05) compared to Normal. Furthermore, correlation analysis revealed a significant positive correlation between glucose metabolism and inflammatory factors, while a negative correlation between mitochondrial function-related genes and fatty acid transport. NGUG piglets showed simultaneous enhancement of glucose uptake and gluconeogenesis, as well as reduced antioxidant capacity and increased inflammatory status, whereas CUG comes at the expense of impaired hepatic mitochondrial function and pathological fat accumulation.

This study was conducted to investigate the effect of dietary Yucca schidigera extract (YSE) supplementation to sow performance, nutrients digestibility and ammonia emission of manure. Total 80 sows were randomly divided into 4 groups and fed with either control, control + 0.06% YSE, control + 0.12% YSE or control + 0.24% YSE diet from day 80 of gestation to day 21 of lactation. The results showed that dietary YSE supplementation resulted in trends toward a reduced number of stillbirth piglets ( P = 0.08), weak piglets (P = 0.06), pre-weanling mortality ( P = 0.04) and diarrhea ( P = 0.03), and improved apparent digestibility of dry matter ( P = 0.04). Besides, YSE supplementation significantly increased catalase activity ( P = 0.02) while decreasing malonaldehyde levels ( P = 0.04) in sow blood. Furthermore, the loss of total nitrogen, urea nitrogen and ammonia nitrogen in sow manure were significantly reduced with supplementation of YSE. In summary, supplementation of YSE in sow diet during late gestation and lactation could improve sow and litter performance, nutrient digestibility, and reduce nitrogen loss in sow manure during storage.

Background Our previous study found that sow dietary leucine supplementation signicicantly improved fetal intrauterine growth and newborn piglet birth weight. But we still have limited knowledge how leucine regulated placental functions to promote the nutrient supply to fetus to support its intrauterine development. Methods 150 sows at day 90 of gestiation were divided into three groups and fed with either control diet (CON), CON + 0.4% Leu or CON + 0.8% Leu separately until parturition. Placental metabolomics, full spectrum amino acids and nutrient transporters were systematically analyzed. Results Leu supplementation lead to an altered placental metabolism with higher amount of metabolites related to glycolysis and fatty acids oxidatation, and more amino acids accumulation in placenta. Besides, nutrient transporters including amino acids transporters, glucose transporters and fatty acids transporters in placenta were globally enhanced and several enzymes related to energy metabolism including hexokinase, succinatede hydrogenase, lactated hydrogenase, glycogen phosphorylase and hydroxyaryl-CoA-dehydrogenase were significantly increased with no change in antioxidative status in the groups with Leu supplementation. Futhermore, Leu supplementation significantly increased phosphalation of PI3K, Akt, and mTOR in placenta compared with control group. Conclusions Leu supplementation during late gestation globally altered placental metabolism, nutrient transport (amino acids, glucose, and fatty acids) via modulation of the PI3K/Akt/mTOR signalling pathway.

(1) Background: Nutritional strategies to enhance gut function and reduce the piglet diarrhea rate are critical to increase the growth performance of piglets. The purpose of this study was to investigate whether dietary fat types and/or fat microencapsulation techniques are involved in regulating the fatty acid transport system and the mechanical and immunological barriers of the small intestine. (2) Methods: Three hundred twenty-four weaning piglets were randomly divided into three groups fed a soybean oil diet (SBO, control group, 6.0% soybean oil), palm oil diet (PO, 6.0% palm oil), or encapsulated palm oil diet (EPO, 7.5% encapsulated palm oil). (3) Results: A significantly lower mRNA expression of the claudin was observed in the duodenum and jejunum of the PO group than in the SBO group (p < 0.05). However, the mRNA expression and protein abundance of claudin and ZO-1 in the jejunum of the EPO group were higher (p < 0.05) than in the PO group. Porcine β-defensin (pBD) secretion was not significantly different between the SBO and PO groups (p > 0.05), while the pBD-2 levels were significantly different (p < 0.05). Compared with the PO group, the EPO group exhibited a significantly increased secretion of pBD-2 and pBD-129 in the small intestine (p < 0.05) and pBD-1 in the jejunum and ileum (p < 0.05). The protein abundances of apolipoprotein AIV (Apo AIV) and intestinal fatty acid binding protein (I-FABP) were significantly lower in the PO group than in the SBO group (p < 0.05). Simultaneously, the protein abundances of fatty acid transport protein 4 (FATP4), fatty acid translocase (CD36), and I-FABP were higher in the EPO group than in the PO group. Furthermore, the low digestibility of palm oil (PO group) might negatively regulate intestinal tight junctions, fatty acid transporters, lipoproteins, and β-defensin through the activation of the AMPK/mTORC1 and AMPK/Sirt1/NF-κB pathways. (4) Conclusions: In summary, microencapsulation techniques might alleviate the negative effects of palm oil and help to improve the intestinal fatty acid transport system and barrier function.