Protective effects of taurine against muscle damage induced by diquat in 35?days weaned piglets.
Ontology highlight
ABSTRACT:
SUBMITTER: Wen C
PROVIDER: S-EPMC7268319 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
Publications
Protective effects of taurine against muscle damage induced by diquat in 35 days weaned piglets.
Wen Chaoyue C Li Fengna F Guo Qiuping Q Zhang Lingyu L Duan Yehui Y Wang Wenlong W Li Jianzhong J He Shanping S Chen Wen W Yin Yulong Y
Journal of animal science and biotechnology 20200603
<h4>Background</h4>Oxidative stress is a key factor that influences piglets' health. Taurine plays an imperative role in keeping the biological system from damage. This study was conducted to investigate the protective effect of taurine against muscle injury due to the secondary effect of diquat toxicity.<h4>Results</h4>Our study found that taurine effectively and dose-dependently alleviated the diquat toxicity induced rise of feed/gain, with a concurrent improvement of carcass lean percentage. ...[more]
Similar Datasets
Project description:The liver is an organ that produces large amounts of reactive oxygen species (ROS). Human infants or piglets are prone to oxidative damage due to their uncompleted development of the antioxidant system, causing liver disease. Piceatannol (PIC) has been found to have significant antioxidant effects. The aim of this experiment was to investigate the effects of PIC on the liver in piglets experiencing oxidative stress caused by diquat (DQ). After weaning, 54 male piglets (Duroc × [Landrace × Yorkshire]) were selected and randomly divided into three treatment groups: the CON group, the DQ-CON group, and the DQ-PIC group. The two challenged groups were injected with DQ and then orally administrated either PIC or another vehicle solution, while the control group was given sterile saline injections and an orally administrated vehicle solution. Compared to the results of the CON group, DQ increased the percentage of apoptosis cells in the liver, also decreased the amount of reduced glutathione (GSH) and increased the concentration of malondialdehyde (MDA). In addition, the adenosine triphosphate (ATP) production, activities of mitochondrial complex I, II, III, and V, and the protein expression level of sirtuin 1 (SIRT1) were inhibited by DQ. Furthermore, PIC supplementation inhibited the apoptosis of hepatic cells caused by DQ. PIC also decreased MDA levels and increased the amount of GSH. Piglets given PIC supplementation exhibited increased activities of mitochondrial complex I, II, III, and V, the protein expression level of SIRT1, and the ATP production in the liver. In conclusion, PIC affected the liver of piglets by improving redox status, preserving mitochondrial function, and preventing excessive apoptosis.
| S-EPMC7401537 | biostudies-literature
Project description:Transcriptional profiling of 25d old piglets comparing control untreated suckling jejunum with weaned piglets' jejunum. The goal was to gain new insight into the interaction between weaning and intestinal function.A keen interest is paid in deciphering expression changes of apoptosis or cell cycle control genes. The statistical analysis of gene ontology revealed that most of these altered genes are metabolic-related enzymes and regulators which may involved in the biological regulation, developmental process, and cellular process. Weaning also causes alterations in various immune response pathways. Results likely indicate that weaning induced cell cycle arrest, enhanced apoptosis, and inhibited cell proliferation.
2014-05-01 | GSE48050 | GEO
Project description:BackgroundEnterotoxigenic Escherichia coli K88 (E. coli K88) are considered as a major cause of diarrhea and death in newly weaned piglets. Oral passive immunization with chicken egg yolk immunoglobulins (IgY) have attracted considerable attention for treatment of gastrointestinal infection due to its high specificity. In this study it was estimated the protective effect of anti-K88 fimbriae IgY against E. coli K88 adhesion to piglet intestinal mucus in vitro and to investigate the potential use of IgY for controlling E. coli-induced diarrhea in weaned piglets in vivo.ResultsE. coli K88 was incubated with IgY for 24 h, and the bacterial growth profiles showed that specific IgY with a concentration higher than 5 mg/mL was observed to significantly inhibit the growth of E. coli K88 compared to nonspecific yolk powder in a liquid medium. Moreover, pretreatment with 50 mg/mL of IgY was found to significantly decrease the adhesion ability of E. coli K88 to porcine jejunal and ileal mucus, further supported by the observations from our immunofluorescence microscopic analysis. In vivo, administration of IgY successfully protected piglets from diarrhea caused by E. coli K88 challenge. Additionally, IgY treatment efficiently alleviated E. coli-induced intestinal inflammation in piglets as the gene expression levels of inflammatory cytokines TNF-α, IL-22, IL-6 and IL-1β in IgY-treated piglets remained unchanged after E. coli K88 infection. Furthermore, IgY significantly prevented E. coli K88 adhering to the jejunal and ileal mucosa of piglets with E. coli infection and significantly decreased E. coli and enterotoxin expression in colonic contents.ConclusionOutcome of the study demonstrated that IgY against the fimbrial antigen K88 was able to significantly inhibit the growth of E. coli K88, block the binding of E. coli to small intestinal mucus, and protect piglets from E. coli-induced diarrhea. These results indicate that passive immunization with IgY may be useful to prevent bacterial colonization and to control enteric diseases due to E. coli infection. The study has great clinical implication to provide alternative therapy to antibiotics in E coli induced diarrhea.
| S-EPMC6615277 | biostudies-literature
Project description:Transcriptional profiling of 25d old piglets comparing control untreated suckling jejunum with weaned piglets' jejunum. The goal was to gain new insight into the interaction between weaning and intestinal function.A keen interest is paid in deciphering expression changes of apoptosis or cell cycle control genes. The statistical analysis of gene ontology revealed that most of these altered genes are metabolic-related enzymes and regulators which may involved in the biological regulation, developmental process, and cellular process. Weaning also causes alterations in various immune response pathways. Results likely indicate that weaning induced cell cycle arrest, enhanced apoptosis, and inhibited cell proliferation. Two-condition experiment, suckling control piglets' jejunum vs. weaned piglets' jejunum. Biological replicates: 4 control replicates, 4 weaned replicates.
2014-05-01 | E-GEOD-48050 | biostudies-arrayexpress
Project description:Lawsoniaintracellularis, which causes porcine proliferative enteropathy (PPE), is a common swine intestinal pathogen that is prevalent in pig production sites worldwide. In this study, the alteration in the microbiome composition of weaned pigs was investigated in response to vaccination against L. intracellularis, using 16S rRNA gene sequencing. A total of 64 crossbred (Duroc × [Landrace × Yorkshire]) healthy weanling pigs weaned at 4 weeks of age were randomly assigned to four treatment groups (four pigs/pen; four pens/treatment), using a randomized complete block design for the 42-day trial. Pigs in the treatment groups were orally administered with three different doses (1 dose = 2 mL) of vaccine against L. intracellularis (Enterisol® Ileitis, Boehringer Ingelheim Vetmedica GmbH), namely the following: LAW1 (0.5 dose), LAW2 (1 dose), LAW3 (2 dose). A non-vaccinated group served as a negative control (CONT). Alpha diversity analysis revealed that vaccination led to significant changes in species evenness but not species richness of the gut microbiota. Beta diversity analysis revealed that vaccination against L. intracellularis caused a significant shift in the microbial community structure. At the genus level, there was a significant increase in Streptococcus and a significant decrease in Clostridium in the fecal microbiota of vaccinated pigs, regardless of dose.
| S-EPMC8300401 | biostudies-literature
Project description:Development of immune competence in pigs is important for resilience, disease resistance, and performance later in life. Dietary interventions in early life can contribute to immune system development. Use of model dietary interventions, such as diets with a high concentration of zinc, can contribute to the understanding of the interactions between the diet, the intestinal microbiota and intestinal tissues. The aim of the present study was to evaluate the effects of provision of a diet with a high concentration of zinc (Zn, 2690 mg/kg), as model intervention, as compared to provision of a control diet with a regular Zn concentration (100 mg/kg) during a period of nine days during the post weaning period (d 14-23 post weaning (pw)), on the composition of the intestinal microbiota and gene expression in the intestinal mucosa on d 23 and 35 pw (12 d after the termination of the Zn intervention). Whole genome gene expression analysis of the jejunal and ileal mucosa revealed a small overall time-treatment interaction effect at d 23 pw in both intestinal tissues. In both jejunal and ileal mucosa various genes/probes were differentially up or down regulated between treatments. In intestinal tissue samples obtained on d 35 no differences in gene expression were observed. Probes of d 23 pw that were differently expressed and had an annotation were subsequently used as input for further functional analysis using DAVID and Gene Decks databases. The analysis did not result in the identification of gene sets that were differentially expressed between dietary treatments. However, it was shown that a number of upregulated genes in the jejunal mucosa on d 23 pw by the high zinc intervention are involved in pathways related to mineral absorption, immune signalling and cell energy metabolism (glycolysis and gluconeogenesis). A few down regulated genes by the Zn intervention are also involved in immune signalling pathways. It was concluded from the present study that provision of a diet with a high concentration of zinc as zinc oxide during a short period of time (9 days) to piglets in the post weaning period (d 14-23 pw) induces differences on the intestinal expression of genes in part related to the functioning of the local innate immune system. The high dietary zinc intervention can therefore be considered as a suitable model for studying relationships between dietary interventions and development of immune competence in post weaning piglets.
2017-04-19 | GSE94370 | GEO
Project description:Melatonin has been reported to play crucial roles in regulating meat quality, improving reproductive properties and maintaining intestinal health in animal production, but whether it regulates skeletal muscle development in weaned piglet is rarely studied. This study was conducted to investigate the effects of melatonin on growth performance, skeletal muscle development and lipid metabolism in animals by intragastric administration of melatonin solution. Twelve 28-day-old DLY (Duroc × Landrace × Yorkshire) weaned piglets with similar body weight were randomly divided into two groups: control group and melatonin group. The results showed that melatonin supplementation for 23 days had no effect on growth performance, but significantly reduced serum glucose content (P<0.05). Remarkably, melatonin increased longissimus dorsi muscle (LDM) weight, eye muscle area and decreased the liver weight in weaned piglets (P<0.05). In addition, the cross-sectional area of muscle fibers was increased (P<0.05), while triglyceride (TG) levels were decreased in LDM and psoas major muscle (PMM) by melatonin treatment (P<0.05). Transcriptome sequencing showed melatonin induced the expression of genes related to skeletal muscle hypertrophy and fatty acid oxidation. Enrichment analysis indicated that melatonin regulated cholesterol metabolism, protein digestion and absorption and mitophagy signaling pathways in muscle. Gene set enrichment analysis (GSEA) also confirmed the effects of melatonin on skeletal muscle development and mitochondrial structure and function. Moreover, quantitative real-time polymerase chain reaction (qPCR) analysis revealed that melatonin supplementation elevated the gene expression of cell differentiation and muscle fiber development, including paired box 7 (PAX7), myogenin (MYOG), myosin heavy chain (MYHC) ⅡA and MYHC ⅡB (P<0.05), which was accompanied by increased insulin like growth factor 1 (IGF1) and insulin like growth factor binding protein 5 (IGFBP5) expression in LDM (P<0.05). Additionally, melatonin regulated lipid metabolism and activated mitochondrial function in muscle by increasing the mRNA abundance of cytochrome c oxidase subunit 6A (COX6A), COX5B and carnitine palmitoyltransferase 2 (CPT2) and decreasing the mRNA expression of peroxisome proliferator activated receptor gamma (PPARG), Acetyl-CoA carboxylase (ACC) and fatty acid binding protein 4 (FABP4) (P<0.05). Together, our results suggest that melatonin could promote skeletal muscle growth and muscle fiber hypertrophy, improve mitochondrial function and decrease fat deposition in muscle.
2023-10-02 | GSE237322 | GEO
Project description:BackgroundIntestinal inflammation is the main risk factor causing intestinal barrier dysfunction and lipopolysaccharide (LPS) can trigger inflammatory responses in various eukaryotic species. Yeast hydrolysate (YH) possesses multi-biological effects and is received remarkable attention as a functional ingredient for improving growth performance and promoting health in animals. However, there is still inconclusive on the protective effects of dietary YH supplementation on intestinal barrier of piglets. This study was conducted to investigate the attenuate effects of YH supplementation on inflammatory responses and intestinal barrier injury in piglets challenged with LPS.MethodsTwenty-four piglets (with an average body weight of 7.42 ± 0.34 kg) weaned at 21 days of age were randomly assigned to one of two dietary treatments (12 replications with one pig per pen): a basal diet or a basal diet containing YH (5 g/kg). On the 22nd d, 6 piglets in each treatment were intraperitoneally injected with LPS at 150 μg/kg BW, and the others were injected with the same amount of sterile normal saline. Four hours later, blood samples of each piglet were collected and then piglets were euthanized.ResultsDietary YH supplementation increased average daily feed intake and average daily gain (P < 0.01), decreased the ratio of feed intake to gain of piglets (P = 0.048). Lipopolysaccharide (LPS) injection induced systemic inflammatory response, evidenced by the increase of serum concentrations of haptoglobin (HP), adrenocorticotropic hormone (ACTH), cortisol, and interleukin-1β (IL-1β). Furthermore, LPS challenge resulted in inflammatory intestinal damage, by up-regulation of the protein or mRNA abundances of tumor necrosis factor-α (TNF-α), IL-1β, toll-like receptors 4 (TLR4) and phosphor-nuclear factor-κB-p65 (p-NFκB-p65) (P < 0.01), and down-regulation of the jejunal villus height, the protein and mRNA abundances of zonula occludens-1 (ZO-1) and occludin (OCC; P < 0.05) in jejunal mucosa. Dietary YH supplementation decreased the impaired effects of ACTH, cortisol, HP, IL-1β and diamine oxidase in serum (P < 0.05). Moreover, YH supplementation also up-regulated the jejunal villus height, protein and mRNA abundances of ZO-1 and OCC (P < 0.05), down-regulated the mRNA expressions of TNF-α and IL-1β and the protein abundances of TNF-α, IL-1β, TLR4 and p-NFκB-p65 in jejunal mucosa in LPS-challenged pigs (P < 0.01).ConclusionYeast hydrolysate could attenuate inflammatory response and intestinal barrier injury in weaned piglets challenged with LPS, which was associated with the inhibition of TLR4/NF-κB signaling pathway activation.
| S-EPMC10021991 | biostudies-literature
Project description:BackgroundEvidence indicates that early weaning predisposes piglets to intestinal oxidative stress and increases the risk of intestinal dysfunction; however, there are minimal satisfactory treatment strategies for these conditions. This study investigated the potential of resveratrol and its analog, pterostilbene, as antioxidant protectants for regulating intestinal morphology, barrier function, and redox status among weanling piglets.MethodsA total of 144 piglets were selected at 21 days of age and randomly allocated into one of four treatment groups, each of which included six replicates. Piglets in a sow-reared control group were suckling normally between ages 21 and 28 days, while those in weaned groups were fed a basal diet, supplemented with either 300 mg/kg of resveratrol or with 300 mg/kg of pterostilbene. Parameters associated with intestinal injury and redox status were analyzed at the end of the feeding trial.ResultsEarly weaning disrupted the intestinal function of young piglets, with evidence of increased diamine oxidase activity and D-lactate content in the plasma, shorter villi, an imbalance between cell proliferation and apoptosis, an impaired antioxidant defense system, and severe oxidative damage in the jejunum relative to suckling piglets. Feeding piglets with a resveratrol-supplemented diet partially increased villus height (P = 0.056) and tended to diminish apoptotic cell numbers (P = 0.084) in the jejunum compared with those fed a basal diet. Similarly, these beneficial effects were observed in the pterostilbene-fed piglets. Pterostilbene improved the feed efficiency of weanling piglets between the ages of 21 and 28 days; it also resulted in diminished plasma diamine oxidase activity and D-lactate content relative to untreated weaned piglets (P < 0.05). Notably, pterostilbene restored jejunal antioxidant capacity, an effect that was nearly absent in the resveratrol-fed piglets. Pterostilbene reduced the malondialdehyde and 8-hydroxy-2´-deoxyguanosine contents of jejunal mucosa possibly through its regulatory role in facilitating the nuclear translocation of nuclear factor erythroid-2-related factor 2 and the expression levels of NAD(P)H quinone dehydrogenase 1 and superoxide dismutase 2 (P < 0.05).ConclusionsThe results indicate that pterostilbene may be more effective than its parent compound in alleviating early weaning-induced intestinal damage and redox imbalance among young piglets.
| S-EPMC7262760 | biostudies-literature
Project description:This investigation evaluated the potential of natural antioxidants, pterostilbene (PT) and its parent compound resveratrol (RSV), to alleviate hepatic damage, redox imbalance, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress in early-weaned piglets. A total of 144 suckling piglets were randomly assigned to four treatments (six replicates per group, n = 6): 1) sow reared, 2) early weaned and fed a basal diet, 3) early weaned and fed the basal diet supplemented with 300 mg/kg PT, or with 4) 300 mg/kg RSV. Early weaning increased plasma alanine aminotransferase (P = 0.004) and aspartate aminotransferase (P = 0.009) activities and hepatic apoptotic rate (P = 0.001) in piglets compared with the sow-reared piglets. Early weaning decreased hepatic adenosine triphosphate (ATP; P = 0.006) content and mitochondrial complexes III (P = 0.019) and IV activities (P = 0.038), but it increased superoxide anion accumulation (P = 0.026) and the expression levels of ER stress markers, such as glucose-regulated protein 78 (P < 0.001), CCAAT/enhancer-binding protein-homologous protein (P = 0.001), and activating transcription factor (ATF) 4 (P = 0.006). PT was superior to RSV at mitigating liver injury and oxidative stress after early weaning, as indicated by decreases in the number of apoptotic cells (P = 0.036) and the levels of superoxide anion (P = 0.002) and 8-hydroxy-2 deoxyguanosine (P < 0.001). PT increased mitochondrial deoxyribonucleic acid content (P = 0.031) and the activities of citrate synthase (P = 0.005), complexes I (P = 0.004) and III (P = 0.011), and ATP synthase (P = 0.041), which may contribute to the mitigation of hepatic ATP deficit (P = 0.017) in the PT-treated weaned piglets. PT also prevented increases in the ER stress marker and ATF 6 expression levels and in the phosphorylation of inositol-requiring enzyme 1 alpha caused by early weaning (P < 0.05). PT increased sirtuin 1 activity (P = 0.031) in the liver of early-weaned piglets than those in the early-weaned piglets fed a basal diet. In conclusion, PT supplementation alleviates liver injury in weanling piglets probably by inhibiting mitochondrial dysfunction and ER stress.
| S-EPMC7603403 | biostudies-literature