This study investigated the effects of dietary esculetin supplementation on growth performance, carcass traits, intestinal morphology, digestive enzymes, barrier function and cecal microbiota in broiler chickens. A total of 960 one-day-old chickens were randomly divided into six groups and fed diets supplemented with different levels of esculetin (0, 10, 25, 50, 75 and 100 mg/kg) for 42 consecutive days. The results showed that esculetin supplementation linearly and quadratically increased average daily gain, and linearly decreased the ratio of feed to gain during d 22-42 and d 1-42. Evisceration rate increased quadratically, and semi-evisceration increased linearly and quadratically with esculetin supplementation. Additionally, esculetin supplementation induced linear and quadratic decreases in abdominal fat rate and thymus index. The ratio of villus height to crypt depth in the duodenal and jejunal increased linearly and quadratically, while duodenal crypt depth decreased linearly. Esculetin supplementation also caused linear and quadratic increases in jejunal villus height. Amylase activity in the duodenum and jejunum increased linearly and quadratically with esculetin supplementation. Jejunal occludin mRNA expression levels increased linearly and quadratically, and esculetin supplementation quadratically increased claudin-1 and trefoil factor 3 mRNA expression levels in both the jejunum and ileum. Dietary esculetin supplementation linearly and quadratically increased ileal immunoglobulin (Ig) M and IgG levels. Moreover, 16S rRNA sequencing revealed that esculetin supplementation modulated the diversity and composition of cecal microflora. Esculetin supplementation significantly increased the relative abundance of Christensenellaceae_R-7_group and decreased the relative abundance of Butyricimonas. Overall, esculetin supplementation enhances growth performance in broiler, probably by improving intestinal morphology, nutrient digestion, barrier function, immune response, and modulating cecal microbiota.

The medicinal herb Artemisia annua L. has traditionally been used to promote human and animal health. One of the most important bioactive metabolites is dihydroartemisinin; however, its impact on intestinal health in broilers has not been sufficiently researched. The aim of this study was to investigate the effects of dihydroartemisinin on growth performance, slaughter performance, serum biochemistry, and intestinal health of AA broiler chickens. Four hundred broilers were randomly divided into five treatment groups, with eight replicates and ten chickens per replicate. The birds were fed a basal diet supplemented with 0, 5, 10, 20, or 40 mg/kg dihydroartemisinin for 42 consecutive days. The data were analyzed by one-way ANOVA and orthogonal polynomial contrast. Results showed that dihydroartemisinin supplementation at 10 mg/kg quadratically increased the average body weight, and supplementation at 10 to 20 mg/k quadratically increased the average daily gain from days 1 to 21. Dihydroartemisinin supplementation at 20 mg/kg quadratically increased the breast muscle rate and relative length of the jejunum (P < 0.05). Dihydroartemisinin supplementation at 5 to 40 mg/kg also quadratically increased the serum total protein, albumin, and IgG concentrations at d 42 (P < 0.05). Dihydroartemisinin supplementation at 5 to 10 mg/kg also quadratically increased the serum globulin concentrations (P < 0.05). Furthermore, dihydroartemisinin supplementation at 10 to 20 mg/kg quadratically improved villus length and the villus length to crypt depth ratio in both the jejunum and ileum, while reducing crypt depth and increasing the thickness of jejunal tunica muscularis (P < 0.05). Dihydroartemisinin supplementation at 10 to 20 mg/kg caused a linear and quadratic increase in the mRNA expression of claudin-1 in the jejunum (P < 0.05), an indicator of positive effects on intestinal tight junctions. Dihydroartemisinin supplementation at 10 to 20 mg/kg also linearly and quadratically increased the mRNA expression of mucin2 (MUC2) and toll-like receptor 4 in the jejunum (P < 0.05). Compared to the control group, dihydroartemisinin supplementation at 5, 20, and 40 mg/kg quadratically increased the mRNA expression of kruppel-like factor 4 (KLF4) in the jejunum (P < 0.05). In conclusion, dihydroartemisinin promoted slaughter performance, serum biochemistry, and intestinal health, including improvements to intestinal morphology and the mucus barrier through the induction of MUC2 and KLF4 genes expression.

This study aimed to investigate the effects of dietary dihydroartemisinin on the growth performance, meat quality, and antioxidant capacity of broiler chickens. Four-hundred one-day-old Arbor Acres male broilers were randomly assigned to five treatment groups with eight replicates and ten birds each. All broilers were fed a basal diet containing 0, 5, 10, 20 or 40 mg/kg dihydroartemisinin. The results showed that dihydroartemisinin at 10 mg/kg quadratically increased ADG, and dihydroartemisinin at 10 and 20 mg/kg quadratically increased ADFI during the days 1-21 period. Compared to the control group, dihydroartemisinin at 10 and 20 mg/kg quadratically decreased the drip loss at 24 h. Dihydroartemisinin linearly and quadratically decreased the L* value of breast muscles. Dihydroartemisinin at 20-40 mg/kg linearly and quadratically decreased the MDA concentrations at D5 and D 7 of postmortem storage. Dihydroartemisinin linearly and quadratically increased the ABTS scavenging activity at D 7 of postmortem storage. Dietary 20 mg/kg dihydroartemisinin at 21 days and 40 mg/kg dihydroartemisinin at 42 days linearly and quadratically increased serum glutathione concentrations. Dihydroartemisinin at 5-40 mg/kg linearly increased serum total superoxide dismutase activity at 42 days. Dihydroartemisinin at 10-20 mg/kg quadratically decreased serum malondialdehyde contents at 42 days. At 21 days, 20 mg/kg dihydroartemisinin quadratically increased hepatic glutathione concentrations and catalase activities. Compared to the control group, 40 mg/kg dihydroartemisinin linearly and quadratically decreased hepatic malondialdehyde contents. At 42 days, 20 mg/kg dihydroartemisinin quadratically increased catalase activities and reduced the malondialdehyde contents in liver. Dihydroartemisinin quadratically increased the hepatic mRNA expression of Nrf2. Compared to the control group, dihydroartemisinin at 10 and 20 mg/kg quadratically induced the hepatic mRNA expression of HO-1. Dihydroartemisinin at 10-40 mg/kg linearly and quadratically increased the mRNA expression of CAT in liver. These results showed that dihydroartemisinin improved growth performance, meat quality, and antioxidant capacity of broiler chickens, especially at 10 and 20 mg/kg.

Lay Summary The intensive breeding model of broilers exposes broilers directly to oxidative stress, which is associated with mitochondrial dysfunction. Some researches have shown that bamboo leaf extract (BLE) exhibited antioxidant capacity both in vitro and vivo. However, few researches have been conducted to explore the effects of BLE supplementation on small intestine mitochondrial functions in broilers. The study aimed to evaluate whether BLE can improve energy metabolism, antioxidant capacity, and biogenesis of broilers' small intestine mitochondria. All broilers were randomly divided into four groups. The control (CTR) group was fed a basal diet, and the three experimental groups of BLE1, BLE2, and BLE3 were fed the basal diet supplemented with 1.0, 2.0, and 4.0 g of BLE per kg of feed between 1 d and 42 d of age, respectively. Based on our results, we obtained interesting evidence that BLE supplementation enhanced metabolic efficiency of small intestine mitochondria in broilers. Bamboo leaf extract supplementation can improve the energy metabolism, antioxidant capacity, and biogenesis of small intestine mitochondria in broilers. The present study was carried out to investigate the effects of bamboo leaf extract (BLE) on energy metabolism, antioxidant capacity, and biogenesis of broilers' small intestine mitochondria. A total of 384 one-day-old male Arbor Acres broiler chicks were randomly divided into four groups with six replicates each for 42 d. The control group was fed a basal diet, whereas the BLE1, BLE2, and BLE3 groups consumed basal diets with 1.0, 2.0, and 4.0 g/kg of BLE, respectively. Some markers of mitochondrial energy metabolism including isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate dehydrogenase and some markers of redox system including total superoxide dismutase, malondialdehyde, and glutathione were measured by commercial colorimetric kits. Mitochondrial and cellular antioxidant genes, mitochondrial biogenesis-related genes, and mitochondrial DNA copy number were measured by quantitative real-time-polymerase chain reaction (qRT-PCR). Data were analyzed using the SPSS 19.0, and differences were considered as significant at P < 0.05. BLE supplementation linearly increased jejunal mitochondrial isocitrate dehydrogenase (P < 0.05) and total superoxide dismutase (P < 0.05) activity. The ileal manganese superoxide dismutase mRNA expression was linearly affected by increased dietary BLE supplementation (P < 0.05). Increasing BLE supplementation linearly increased jejunal sirtuin 1 (P < 0.05) and nuclear respiratory factor 1 (P < 0.05) mRNA expression. Linear (P < 0.05) and quadratic (P < 0.05) responses of the ileal nuclear respiratory factor 2 mRNA expression occurred with increased dietary BLE levels. In conclusion, BLE supplementation was beneficial to the energy metabolism, antioxidant capacity, and biogenesis of small intestine mitochondria in broilers. The dose of 4.0 g/kg BLE demonstrated the best effects.

Heat stress (HS) can lead to oxidative stress (OS), which jeopards human health and animal production. Capsaicin (CAP) has antioxidant activities. This study aimed to investigate the impacts of CAP on the alleviation of intestinal OS in heat-stressed mice. All 40 male C57BL/6J mice were randomly allotted to 4 groups in a 2 × 2 factorial arrangement with 2 levels of CAP (0 and 0.4 mg/d for 15 days) and 2 ambient temperatures (normal and HS (39.5 °C per day for 2 h for the last 6 days) conditions). CAP treatment enhanced the villus height under HS conditions. CAP supplementation increased serum superoxide dismutase (SOD) activity, jejunal glutathione peroxidase (GPX) activity, and HO-1, SOD1, SOD2, and GPX1 gene abundance, also upregulated TRPV1 and UCP2 expressions in heat-stressed mice. Meanwhile, CAP administration reversed the HS-induced elevation of the TNF-α and IFN-γ abundance. Collectively, CAP could enhance intestinal antioxidant capacity in heat-stressed mice.

当前我国养猪业和饲料业正面临疫病频发、蛋白原料紧缺、高同源蛋白风险、饲料、养殖和人工成本持续升高等种种难题,当前国内蛋白原料匮乏,已经是行业不可忽视的难题.据农业农村部统计, 2017 年我国的蛋白饲料进口来源占比约 95％,鱼粉进口来源占比约80％,开发优质蛋白原料,高效利用现有的蛋白资源,是饲料工业的趋势.

Intra-uterine growth restriction (IUGR) is a serious, commonly occurring reproductive problem in humans. This study aimed to investigate the effects of daily curcumin supplementation during pregnancy on placental inflammation, in a rat model of IUGR. Pregnant rats were divided into three groups based on diet: (1) normal protein (19%) (NP), (2) low protein (8%) (LP), and (3) low protein + 100 mg curcumin/kg bw per day (LPC). The results showed that curcumin accumulation in the serum, placenta and liver. Fetal weight and placental total protein levels were increased in the LPC group compared with those in the LP group. Dietary curcumin supplementation normalized the low protein diet-induced decrease of placental weight, blood sinusoid area, and proliferating cell nuclear antigen (PCNA) protein expression levels. It also reversed the low protein diet-induced increase of serum triglyceride levels and tumor necrosis factor alpha-like (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) concentrations in both the placenta and serum. Additionally, it normalized the enhanced gene expression levels of the pro-inflammatory cytokines in the LP group to that in the NP group. Furthermore, it downregulated the inhibitor of kappa Balpha (IκBα) and nuclear factor kappa Balpha (NF-κB) phosphorylation. In conclusion, daily curcumin supplementation ameliorates placental inflammation in rats with IUGR by inhibiting the NF-κB signaling pathway.

Our results showed that dietary leucine supplementation regulated protein metabolism via enhanced mammalian/mechanistic target of rapamycin phosphorylation to promote protein synthesis in response to intrauterine growth restriction (IUGR) in weaned piglets. This provides a reference for dietary manipulation of leucine to minimize the adverse effects of IUGR on protein anabolism and catabolism in the liver. Neonatal piglets often suffer low birth weights and poor growth performance accompanied by the disruption of protein metabolism, when intrauterine growth restriction (IUGR) takes place during pregnancy, leading to a higher mortality and bigger economic loss than expected. Leucine has been proposed to function as a nutritional signal-regulating protein synthesis in numerous studies. The aim of this study was to determine the effect of dietary leucine supplementation on the blood parameters and hepatic protein metabolism in IUGR piglets. Weaned piglets were assigned to one of four treatments in a 2 x 2 factorial arrangement: 1) piglets fed a basal diet with normal birth weight, 2) piglets fed a basal diet plus 0.35% l-leucine with normal birth weight, 3) IUGR piglets fed a basal diet with low birth weight, and 4) IUGR piglets fed a basal diet plus 0.35% l-leucine with low birth weight. The results showed that IUGR decreased serum aspartate aminotransferase and alkaline phosphatase activities and increased serum cortisol and prostaglandin E2 levels at 35 d of age (P < 0.05), suggesting the occurrence of liver dysfunction and stress response. Leucine supplementation increased serum alkaline phosphatase activity and decreased serum cortisol levels at 35 d of age (P < 0.05). IUGR decreased the lysozyme activity and complement 3 level in serum (P < 0.05), which were prevented by dietary leucine supplementation. IUGR piglets showed increased hepatic DNA contents while showing a reduced RNA/DNA ratio (P < 0.05). Piglets supplied with leucine had decreased RNA/DNA ratio in the liver (P < 0.05). Leucine supplementation stimulated hepatic protein anabolism through upregulating protein synthesis-related genes expression and activating the phosphorylation of mammalian/mechanistic target of rapamycin (mTOR) (P < 0.05). Moreover, IUGR inhibited the mRNA expression of hepatic protein degradation-related genes, indicating a compensatory mechanism for the metabolic response. Dietary leucine supplementation attenuated the suppression of the protein catabolism induced by IUGR in the liver. These results demonstrate that dietary leucine supplementation could alter the blood parameters and alleviated the disrupted protein metabolism induced by IUGR via enhanced mTOR phosphorylation to promote protein synthesis in weaned piglets. Lay Summary Intrauterine growth restriction (IUGR) produces a notable disturbance of protein metabolism in piglets, leading to lower birth weights and economic loss. Leucine supplementation positively regulates protein metabolism in animals and has the potential to recover the impaired balance between protein synthesis and degradation. Our study showed that leucine supplementation alleviated the abnormal changes in blood parameters and stimulated protein synthesis through the mammalian/mechanistic target of rapamycin signal pathway in the liver. Leucine supplementation attenuated the suppression of protein degradation induced by IUGR, which might be involved in a hepatic compensatory mechanism contributing to health status.

Our previous study showed that bisdemethoxycurcumin (BUR) exerts anti-inflammatory properties in lipopolysaccharide-induced intestinal injury, and studies have revealed that NOD-like receptor superfamily, pyrin domain containing 3 (NLRP3) inflammasome activation plays a vital role in the pathogenesis of colitis. However, it is not clear whether BUR could attenuate colitis-mediated intestinal inflammation via NLRP3 inflammasome inactivation and modulate the gut microbiota dysbiosis. The results demonstrated that BUR attenuated DSS-induced body weight decrease, histopathological changes, and epithelial apoptosis. BUR significantly improved the intestinal barrier defects and abrogated DSS-induced inflammatory response. Consistently, BUR reduced the expression of NLRP3 family members, confirming its inhibitory effects on NLRP3 inflammasome activation and pyroptosis. BUR regulated microbiota dysbiosis and altered the gut microbial community. BUR supplementation enriched the relative abundance of beneficial bacteria (such as Lactobacillus and Bifidobacterium), which showed significant negative correlations with the pro-inflammatory biomarkers. Collectively, these findings illustrated that BUR could ameliorate DSS-induced colitis by improving intestinal barrier function, reducing apoptosis, inhibiting NLRP3 inflammasome activation, and regulating the gut microbiota.

The present study investigated whether maternal curcumin supplementation might protect against intra-uterine growth retardation (IUGR) induced intestinal damage and modulate gut microbiota in male mice offspring. In total, 36 C57BL/6 mice (24 females and 12 males, 6–8 weeks old) were randomly divided into three groups based on the diet before and throughout pregnancy and lactation: (1) normal protein (19%), (2) low protein (8%), and (3) low protein (8%) + 600 mg kg−1 curcumin. Offspring were administered a control diet until postnatal day 35. Maternal curcumin supplementation could normalize the maternal protein deficiency-induced decrease in jejunal SOD activity (NP = 200.40 ± 10.58 U/mg protein; LP = 153.30 ± 5.51 U/mg protein; LPC = 185.40 ± 9.52 U/mg protein; P < 0.05) and T-AOC content (NP = 138.90 ± 17.51 U/mg protein; LP = 84.53 ± 5.42 U/mg protein; LPC = 99.73 ± 12.88 U/mg protein; P < 0.05) in the mice offspring. Maternal curcumin supplementation increased the maternal low protein diet-induced decline in the ratio of villus height-to-crypt depth (NP = 2.23 ± 0.19; LP = 1.90 ± 0.06; LPC = 2.56 ± 0.20; P < 0.05), the number of goblet cells (NP = 12.72 ± 1.16; LP = 7.04 ± 0.53; LPC = 13.10 ± 1.17; P < 0.05), and the ratio of PCNA-positive cells (NP = 13.59 ± 1.13%; LP = 2.42 ± 0.74%; LPC = 6.90 ± 0.96%; P < 0.05). It also reversed the maternal protein deficiency-induced increase of the body weight (NP = 13.00 ± 0.48 g; LP = 16.49 ± 0.75 g; LPC = 10.65 ± 1.12 g; P < 0.05), the serum glucose levels (NP = 5.32 ± 0.28 mmol/L; LP = 6.82 ± 0.33 mmol/L; LPC = 4.69 ± 0.35 mmol/L; P < 0.05), and the jejunal apoptotic index (NP = 6.50 ± 1.58%; LP = 10.65 ± 0.75%; LPC = 5.24 ± 0.71%; P < 0.05). Additionally, maternal curcumin supplementation enhanced the gene expression level of Nrf2 (NP = 1.00 ± 0.12; LP = 0.73 ± 0.10; LPC = 1.34 ± 0.12; P < 0.05), Sod2 (NP = 1.00 ± 0.04; LP = 0.85 ± 0.04; LPC = 1.04 ± 0.04; P < 0.05) and Ocln (NP = 1.00 ± 0.09; LP = 0.94 ± 0.10; LPC = 1.47 ± 0.09; P < 0.05) in the jejunum. Furthermore, maternal curcumin supplementation normalized the relative abundance of Lactobacillus (NP = 31.56 ± 6.19%; LP = 7.60 ± 2.33%; LPC = 17.79 ± 2.41%; P < 0.05) and Desulfovibrio (NP = 3.63 ± 0.93%; LP = 20.73 ± 3.96%; LPC = 13.96 ± 4.23%; P < 0.05), and the ratio of Firmicutes/Bacteroidota (NP = 2.84 ± 0.64; LP = 1.21 ± 0.30; LPC = 1.79 ± 0.15; P < 0.05). Moreover, Lactobacillus was positively correlated with the SOD activity, and it was negatively correlated with Il − 1β expression (P < 0.05). Desulfovibrio was negatively correlated with the SOD activity and the jejunal expression of Sod1, Bcl − 2, Card11, and Zo − 1 (P < 0.05). Maternal curcumin supplementation could improve intestinal integrity, oxidative status, and gut microbiota in male mice offspring with IUGR.

This experiment was conducted to investigate the effects of capsaicin (CAP) on growth performance, meat quality, digestive enzyme activities, intestinal morphology, and organ indexes of broilers. A total of 256 one-day-old Arbor Acre male broilers were randomly allocated into four treatments with eight replicates of eight birds, feeding a basal diet (control group), a basal diet supplemented with 2, 4, and 6 mg/kg CAP for 42 d, respectively. The growth performance, digestive enzyme activities of intestinal contents, small intestinal morphology, and organ indexes were measured at 21 and 42 d. The meat quality traits of breast muscles were determined at 42 d. The results showed dietary 4 mg/kg CAP supplementation decreased (P < 0.05) the feed to gain ratio (F/G) in the grower phase (22-42 d) and overall (1-42 d) compared with the control group, and 2 mg/kg CAP group also decreased (P < 0.05) the F/G from 1 to 42 d. Dietary 4 mg/kg CAP supplementation decreased (P < 0.05) the drip loss at 48 h and the pH(24h) of breast muscles relative to the control group. Some digestive enzymes activities of jejunal and ileal contents were increased in the 2 and 4 mg/kg CAP groups compared with the control group both at 21 and 42 d. In addition, dietary 2 mg/kg CAP supplementation increased (P < 0.05) the relative weight of liver, jejunal villus height, villus width, and villous surface area at 21 d; The length of the jejunum segment and the relative weight of Bursa of Fabricius at 42 d in the 4 mg/kg CAP group were higher (P < 0.05) than the control group. In conclusion, dietary 2 or 4 mg/kg CAP supplementation decreased the F/G, improved meat quality, enhanced digestive enzyme activities, improved the jejunal development, and increased the relative liver and Bursa of Fabricius weight in broilers.

The current study sought to understand the mechanism underlying skeletal muscle dysfunction brought on by intrauterine growth restriction (IUGR) and to explore the treatment benefits of applying dimethylglycine sodium salt (DMG-Na) in sow milk to newborns during the suckling period. Each of the 10 sows delivered one newborn with a normal birth weight (NBW) and one with an IUGR. Additionally, two NBW and two IUGR newborns were collected per litter of another 10 sows. The 20 NBW newborns were divided between the N (sow milk) and ND (sow milk + 0.1% DMG-Na) groups, while 20 IUGR newborns were divided between the I (sow milk) and ID (sow milk + 0.1% DMG-Na) groups. The skeletal muscle histomorphology, redox status, and levels of gene and protein expression were worse (p < 0.05) in the I group than in the N group. In addition, supplementation with DMG-Na (ND and ID groups) improved (p < 0.05) those parameters compared to the unsupplemented groups (N and I groups). Inhibited nuclear factor erythroid 2-related factor 2 (Nrf2)/sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptorγcoactivator-1α (PGC-1α) activity resulted in decreased redox status, skeletal muscle structural damage, skeletal muscle mitochondrial function impairment, and decreased performance in IUGR newborns. Supplementation of DMG-Na in sow milk activated the Nrf2/SIRT1/PGC-1α in IUGR newborns, thereby improving their skeletal muscle performance.

[目的]本试验旨在探讨宫内发育迟缓(intrauterine growth retardation,IUGR)对猪胎盘细胞增殖、凋亡及抗氧化基因和蛋白表达的影响.[方法]从刚分娩的母猪中选择正常初生重(normal birth weight,NBW)和IUGR仔猪对应的胎盘各5个,分为对照组和宫内发育迟缓组.采用免疫组化法检测胎盘细胞增殖细胞核抗原(PCNA)的表达,采用TUNEL法检测胎盘细胞凋亡,采用荧光定量PCR检测胎盘NRF2、HO-1、NQO1、SOD1、SOD2、GCLC和GCLM基因的表达,用Westen blot(WB)检测胎盘抗氧化蛋白NRF2和HO-1的表达.[结果]对照组可以观察到较强的PCNA染色,宫内发育迟缓组PCNA染色较弱.IUGR组和对照组凋亡细胞指数分别为19.63％与12.56％,IUGR组细胞凋亡率明显高于对照组(P<0.05).RT-qPCR结果表明,与对照组相比,宫内发育迟缓猪胎盘NRF2、NQO1、SOD1、SOD2、GCLC、GCLM mRNA的表达量显著降低(P<0.05),HO-1 mRNA的表达在正常猪胎盘和宫内发育迟缓猪胎盘组间差异不显著(P>0.05).WB结果显示,对照组与宫内发育迟缓组NRF2和HO-1蛋白表达量差异不显著(P>0.05).[结论]IUGR会降低猪胎盘细胞增殖,增加猪胎盘细胞凋亡且降低猪胎盘抗氧化基因的表达.

The objectives of this study were focused on the mechanism of mitochondrial dysfunction in skeletal muscle stem cells (MuSCs) from intrauterine growth restriction (IUGR) newborn piglets, and the relief of dimethylglycine sodium salt (DMG-Na) on MuSCs mitochondrial dysfunction by Nrf2/SIRT1/PGC1 alpha network. In this study, six newborn piglets with normal birth weight (NBW) and six IUGR newborn piglets were slaughtered immediately after birth to obtain longissimus dorsi muscle (LM) samples. MuSCs were collected and divided into three groups: MuSCs from NBW newborn piglets (N), MuSCs from IUGR newborn piglets (I), and MuSCs from IUGR newborn piglets with 32 mu mol DMG-Na (ID). Compared with the NBW group, the IUGR group showed decreased (P < 0.05) serum and LM antioxidant defense capacity, and increased (P < 0.05) serum and LM damage. Compared with the N group, the I group showed decreased (P < 0.05) MuSCs antioxidant defense capacity, mitochondrial ETC complexes, energy metabolites, and antioxidant defense-related and mitochondrial function-related gene and protein expression levels. The antioxidant defense capacity, mitochondrial ETC complexes, energy metabolites, and antioxidant defense-related and mitochondrial function-related gene and protein expression levels of MuSCs were improved (P < 0.05) in the ID group compared to those in the I group. The MuSCs of IUGR newborns activate the Nrf2/SIRT1/PGC1 alpha network by taking in DMG-Na, thereby neutralizing excessive generated O-2(center dot-) that may help to improve their unfavorable mitochondrial dysfunction in skeletal muscle.

There are few studies on the mechanism of redox status imbalance and intestinal dysfunction in intrauterine growth restricted (IUGR) newborn piglets. Here, we investigated the mechanism of jejunum dysfunction in weaned piglets with IUGR and the mechanism through which dimethylglycine sodium salt (DMG-Na) supplementation improving the imbalance of their redox status. In this work, a total of 10 normal birth weight (NBW) newborn piglets and 20 IUGR newborn piglets were obtained. After weaning at 21 d, they were assigned to 3 groups (n = 10/group): NBW weaned piglets fed standard basal diets (NBWC); one IUGR weaned piglets fed standard basal diets (IUGRC); another IUGR weaned piglets from the same litter fed standard basal diets plus 0.1% DMG-Na (IUGRD). The piglets in these 3 groups were sacrificed at 49 d of age, and the blood and jejunum samples were collected immediately. The growth performance values in the IUGRC group were lower (P < 0.05) than those in the NBWC group. Jejunum histomorphological parameters, inflammatory cytokines, and digestive enzyme activity as well as serum immunoglobulin were lower (P < 0.05) in the IUGRC group than those in the NBWC group. Compared with these in the NBWC group, the redox status of serum, jejunum, and mitochondria and the expression levels of jejunum redox status-related, cell adhesion-related, and mitochondrial function-related genes and proteins were suppressed in the IUGRC group (P < 0.05). However, compared with those in the IUGRC group, the growth performance values, jejunum histomorphological parameters, inflammatory cytokines, digestive enzyme activity, serum immunoglobulin, redox status of serum, jejunum, and mitochondria, and the expression levels of jejunum redox status-related, cell adhesion-related, and mitochondrial function-related genes and proteins were improved (P < 0.05) in the IUGRD group. In conclusion, dietary DMG-Na supplementation alleviates redox status imbalance and intestinal dysfunction in IUGR weaned piglets mainly by activating the sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptorγcoactivator-1α (PGC1α) pathway, thereby improving their unfavorable body state.

Bisdemethoxycurcumin has good antioxidant and anti-inflammatory effects and has been widely used as food and feed supplements in the form of curcuminoids. However, the beneficial effect of individual bisdemethoxycurcumin on preventing lipopolysaccharide (LPS)-induced inflamed intestinal damage is unclear. The present study aimed to investigate whether dietary bisdemethoxycurcumin supplementation could attenuate LPS-induced intestinal damage and alteration of cecal microbiota in broiler chickens. In total, 320 one-day-old male Arbor Acres broiler chickens with a similar weight were randomly divided into four treatments. The treatments were designed as a 2 × 2 factorial arrangement: basal diet (CON); 150 mg/kg bisdemethoxycurcumin diet (BUR); LPS challenge + basal diet (LPS); LPS challenge + 150 mg/kg bisdemethoxycurcumin diet (L-BUR). Results showed that dietary bisdemethoxycurcumin supplementation attenuated the LPS-induced decrease of average daily feed intake. LPS challenge compromised the intestinal morphology and disrupted the intestinal tight junction barrier. Dietary bisdemethoxycurcumin supplementation significantly increased villus length:crypt depth ratio and upregulated the mRNA expression of intestinal tight junction proteins. Moreover, a remarkably reduced mRNA expression of inflammatory mediators was observed following bisdemethoxycurcumin supplementation. The cecal microbiota analysis showed that bisdemethoxycurcumin supplementation increased the relative abundance of the genus Faecalibacterium while decreased the relative abundance of the genera Bacteroides and Subdoligranulum. In conclusion, dietary bisdemethoxycurcumin supplementation could counteract LPS-induced inflamed intestinal damage in broiler chickens by improving intestinal morphology, maintaining intestinal tight junction, downregulating pro-inflammatory mediators, and restoring cecal microbiota.

以肉仔鸡为模型,通过在日粮中添加高剂量竹叶提取物(BLE),研究其对肉鸡生长性能、血常规、血清生化指标和组织病理学的影响,探讨BLE作为肉鸡饲料添加剂使用的安全性.选择体重相近、1日龄的爱拔益佳(AA)肉鸡320只,随机分为4组,每组8个重复,每个重复10只鸡.对照组饲喂基础日粮,试验组分别在基础日粮中添加0.30％、1.50％和3.00％的BLE(1.50％和3.00％为高剂量),试验分为前期1～21 d和后期22～35 d,共35d.结果:与对照组相比,日粮添加高剂量BLE可显著提高后期肉鸡平均日采食量与平均日增重,且线性升高显著(P＜0.05);添加BLE对肉鸡器官指数无显著影响(P＞0.05);此外,高剂量组肉鸡前期血小板数目显著低于对照组,但平均血小板体积显著提高(P＜0.05),添加高剂量BLE对肉鸡后期血常规指标无显著影响(P＞0.05).试验前期,与对照组相比,日粮添加BLE可显著降低肉鸡血清总胆固醇含量,且线性降低显著(P＜0.05);0.30％和3.00％组肉鸡血清谷氨酸氨基转移酶显著低于对照组(P＜0.05);试验后期,与对照组相比,0.30％和3.00％组肉鸡血清白蛋白含量显著升高,高剂量组肉鸡血清血糖含量显著升高(P＜0.05).组织切片观察发现BLE未对组织造成病理伤害.综上,当BLE添加量为3.00％时未对肉鸡机体发育、代谢以及器官功能与结构造成不良影响,肉鸡对其具有一定的耐受性,可作为一种安全肉鸡饲料添加剂使用.

Abstract Background Few studies are available on the mechanism of intestinal dysfunction in newborn piglets with intrauterine growth restriction (IUGR). This work aimed to study the mechanism of jejunum dysfunction in IUGR newborn piglets through RNA-seq and improve their performance by dimethylglycine sodium salt (DMG-Na) supplementation after weaning. Methods In total, 13 normal birth weight (NBW) newborn piglets and 23 IUGR newborn piglets were obtained. Among them, 3 NBW and 3 IUGR newborn piglets were selected and stunned by electric shock after birth without suckling and collected the jejunum samples for RNA-sEq. After weaning at 21 days, they were randomly assigned to 3 groups (n = 10): NBW weaned piglets fed with common basal diets (N); IUGR weaned piglets fed with common basal diets (I); IUGR weaned piglets fed with common basal diets plus 0.1% DMG-Na (ID). All piglets are slaughtered at 49 days of age to collect serum and jejunum samples. Results The hub genes, including ATP8, C11orf86, CDKN1C, DDX58. HPX, INHBB, LECT2, ND1, NFIX, PRDM5, PSD3, SCD, and ZNF770, were found from the data analyzed by RNA-seq and WGCNA. Interestingly, we found ATP8 was the most significantly changed gene, which was crucial in maintaining mitochondrial function. After weaning, the growth performance of ID group was improved (P < 0.05) compared to that in I group. Jejunum histological morphology and its sub-organelle ultrastructure, serum immunoglobulin, jejunum sIgA level, and jejunum digestive enzyme activity were improved (P < 0.05) in ID group compared to those in I group. The redox status of serum, jejunum and its mitochondrial, as well as jejunum redox status-related and mitochondrial function-related gene expression level and protein content were improved (P < 0.05) in ID group in comparison to those in I group. Conclusion The activity of the SIRT1/PGC1α pathway was inhibited in the IUGR weaned piglets, which in turn leads to damage to their redox status and jejunum structure and function, and finally lowers their performance. The IUGR weaned piglets activate the SIRT1/PGC1α pathway by taking in the antioxidant substance like DMG-Na, thereby improving their unfavorable body state.

Bisdemethoxycurcumin is one of the three curcuminoids of turmeric and exhibits good antioxidant activity in animal models. This study is aimed at investigating the effect of bisdemethoxycurcumin on small intestinal mitochondrial dysfunction in lipopolysaccharide- (LPS-) treated broilers, especially on the mitochondrial thioredoxin 2 system and mitochondrial biogenesis. A total of 320 broiler chickens were randomly assigned into four experimental diets using a 2 × 2 factorial arrangement with diet (0 and 150 mg/kg bisdemethoxycurcumin supplementation) and stress (saline or LPS challenge) for 20 days. Broilers received a dose of LPS (1 mg/kg body weight) or sterile saline intraperitoneally on days 16, 18, and 20 of the trial. Bisdemethoxycurcumin mitigated the mitochondrial dysfunction of jejunum and ileum induced by LPS, as evident by the reduced reactive oxygen species levels and the increased mitochondrial membrane potential. Bisdemethoxycurcumin partially reversed the decrease in the mitochondrial DNA copy number and the depletion of ATP levels. Bisdemethoxycurcumin activated the mitochondrial antioxidant response, including the prevention of lipid peroxidation, enhancement of manganese superoxide dismutase activity, and the upregulation of the mitochondrial glutaredoxin 5 and thioredoxin 2 system. The enhanced mitochondrial respiratory complex activities in jejunum and ileum were also attributed to bisdemethoxycurcumin treatment. In addition, bisdemethoxycurcumin induced mitochondrial biogenesis via transcriptional regulation of proliferator-activated receptor-gamma coactivator-1alpha pathway. In conclusion, our results demonstrated the potential of bisdemethoxycurcumin to attenuate small intestinal mitochondrial dysfunction, which might be mediated via activating the mitochondrial antioxidant system and mitochondrial biogenesis in LPS-treated broilers.

Abstract Background: Few studies are available on intestinal barrier function in newborn piglets with intrauterine growth restriction (IUGR). Therefore, this study aimed to investigate the mechanism of intestinal dysfunction in IUGR suckling piglets and improve their growth performance using dimethylglycine sodium salt (DMG-Na) supplementation.Results: The body weights of piglets in the I and ID groups were similar, and both were lower than those in the N and ND groups. However, after 17 days of age, the ID group showed larger (P < 0.05) increases in body weight than did the I group. The hub genes were identified from the data analyzed using RNA-seq and WGCNA. Among these, ATP8 was the most significantly changed, and this gene is crucial in maintaining mitochondrial function. The small intestinal histological morphology, redox status, mitochondrial redox status, oxidative damage, and gene and protein expression levels were worse in the IUGR group than in the NBW group. An increasing trend of the small intestinal histological morphology, redox status, mitochondrial redox status, oxidative damage, and gene and protein expression levels was found between the newborn piglets of the NBW and IUGR groups and the day 21 piglets of the N and I groups, respectively. In addition, supplementation of DMG-Na (ND and ID groups) improved the small intestinal histological morphology, redox status, mitochondrial redox status, oxidative damage, and gene and protein expression levels relative to the non-supplemented groups (N and I groups).Conclusions: The activity of SIRT1/PGC1α was inhibited in IUGR newborn piglets, which led to damage to their intestinal redox status and structure and barrier functions, and lowered their performance. Supplementation with antioxidant substances such as DMG-Na activated SIRT1/PGC1α in IUGR piglets, thereby improving their body state.