Dietary tryptophan improves growth and intestinal health by promoting the secretion of intestinal ß-defensins against enterotoxigenic Escherichia coli F4 in weaned piglets.

Adequate dietary L-tryptophan (Trp) governs intestinal homeostasis in piglets. However, the defensive role of Trp in the diet against enterotoxigenic Escherichia coli F4 (K88) in pigs is still poorly understood. Here, sixty (6.15 ± 1.52 kg, 24-day-old, Duroc × Landrace × Yorkshire) weaned piglets were used for an E. coli F4 attack test in a 2 × 2 factorial design. The growth (ADG, ADFI, GH), immune factors (IL-10, IgA, IgG, IgM), Trp metabolite 5-HT, intestinal morphology (jejunal and colonic VH), mRNA expression of ß-defensins (jejunal BD-127, BD-119, ileal BD-1, BD-127), and abundance of beneficial microorganisms in the colon (Prevotella 9, Lactobacillus, Phascolarctobacterium, Faecalibacterium) were higher in the piglets in the HT (High Trp) and HTK (High Trp, K88) groups than in the LT (Low Trp) and LTK (Low Trp, K88) groups (P<.05), while FCR, diarrhea rate, diarrhea index, serum Trp, Kyn, IDO, D-LA, ET, and abundance of harmful microorganisms in the colon (Spirochaetes, Fusobacteria, Prevotella, Christensenellaceae R7) were lower in the HT and HTK groups than in the LT and LTK groups (P<.05). High Trp reduced the expression of virulence genes (K88 and LT) after E. coli F4 attack (P<.05). The IL-6, TNF-α was lower in the HTK group than in the LT, LTK group (P<.05). In short, a diet containing 0.35% Trp protected piglets from enterotoxigenic E. coli F4 (K88) via Trp metabolism promoting BD expression in the intestinal mucosa, which improved growth and intestinal health.

Diarrhea induced by insufficient fat absorption in weaned piglets: Causes and nutrition regulation.

Fat is one of the three macronutrients and a significant energy source for piglets. It plays a positive role in maintaining intestinal health and improving production performance. During the weaning period, physiological, stress and diet-related factors influence the absorption of fat in piglets, leading to damage to the intestinal barrier, diarrhea and even death. Signaling pathways, such as fatty acid translocase (CD36), pregnane X receptor (PXR), and AMP-dependent protein kinase (AMPK), are responsible for regulating intestinal fat uptake and maintaining intestinal barrier function. Therefore, this review mainly elaborates on the reasons for diarrhea induced by insufficient fat absorption and related signaling pathways in weaned-piglets, with an emphasis on the intestinal fat absorption disorder. Moreover, we focus on introducing nutritional strategies that can promote intestinal fat absorption in piglets with insufficient fat absorption-related diarrhea, such as lipase, amino acids, and probiotics.

Single-cell profiling reveals kidney CD163+ dendritic cell participation in human lupus nephritis.

OBJECTIVES: The current work aimed to provide a comprehensive single-cell landscape of lupus nephritis (LN) kidneys, including immune and non-immune cells, identify disease-associated cell populations and unravel their participation within the kidney microenvironment. METHODS: Single-cell RNA and T cell receptor sequencing were performed on renal biopsy tissues from 40 patients with LN and 6 healthy donors as controls. Matched peripheral blood samples from seven LN patients were also sequenced. Multiplex immunohistochemical analysis was performed on an independent cohort of 60 patients and validated using flow cytometric characterisation of human kidney tissues and in vitro assays. RESULTS: We uncovered a notable enrichment of CD163+ dendritic cells (DC3s) in LN kidneys, which exhibited a positive correlation with the severity of LN. In contrast to their counterparts in blood, DC3s in LN kidney displayed activated and highly proinflammatory phenotype. DC3s showed strong interactions with CD4+ T cells, contributing to intrarenal T cell clonal expansion, activation of CD4+ effector T cell and polarisation towards Th1/Th17. Injured proximal tubular epithelial cells (iPTECs) may orchestrate DC3 activation, adhesion and recruitment within the LN kidneys. In cultures, blood DC3s treated with iPTECs acquired distinct capabilities to polarise Th1/Th17 cells. Remarkably, the enumeration of kidney DC3s might be a potential biomarker for induction treatment response in LN patients. CONCLUSION: The intricate interplay involving DC3s, T cells and tubular epithelial cells within kidneys may substantially contribute to LN pathogenesis. The enumeration of renal DC3 holds potential as a valuable stratification feature for guiding LN patient treatment decisions in clinical practice.

Dietary Soybean Oligosaccharides Addition Increases Growth Performance and Reduces Lipid Deposition by Altering Fecal Short-Chain Fatty Acids Composition in Growing Pigs.

One hundred and twenty-eight boars and gilts of the Duroc × Landrace × Yorkshire variety with an initial body weight (BW) of 52.49 ± 0.48 kg were used in a randomized complete block design for a 63-day experiment. The four treatment groups were: control diet (CON), CON + 0.2% soybean oligosaccharides (SBOS), CON + 0.4% SBOS, and CON + 0.8% SBOS. The results showed that the average daily weight gain (ADG) was significantly higher in the 0.8% SBOS group than in the CON group on days 0-63 (p < 0.05). Compared with the CON group, adding 0.8% SBOS to the diet significantly increased the carcass weight, dressing percentage, and carcass lean percentage, but decreased the average backfat depth of growing-finishing pigs (p < 0.05). Adding different concentrations (0.2%, 0.4%, and 0.8%) of SBOS to the diet can significantly increase the concentrations of acetate, propionate, and butyrate in feces (p < 0.05). The activities of malic enzyme and fatty acid synthase in the 0.8% group were significantly lower than those in the 0.2% and CON groups (p < 0.05). In summary, 0.8% SBOS supplementation to growing-finishing pigs' diets can reduce lipid deposition and increase ADG.

Dietary Taurine Improves Growth Performance and Intestine Health via the GSH/GSSG Antioxidant System and Nrf2/ARE Signaling Pathway in Weaned Piglets.

Early weaning of piglets was prone to increase reactive oxygen species, disrupt the redox balance, decrease antioxidant capacity, cause oxidative stress and intestinal oxidative damage, and lead to diarrhea in piglets. This research aimed to study dietary taurine (Tau) supplementation at a level relieving intestinal oxidative damage in early-weaned piglets. A total of 48 piglets were assigned to four groups of 12 individuals and fed a basal diet with 0.0% Tau (CON), 0.2% Tau (L-Tau), 0.3% Tau (M-Tau), or 0.4% Tau (H-Tau), respectively. The animal experiment lasted 30 days. The final weight, weight gain, average daily gain, and feed conversion rate increased with the increase in dietary Tau (Linear, p < 0.05; Quadratic p < 0.05), while the diarrhea index of piglets decreased with the increase in dietary Tau (Linear, p < 0.05). Serum malondialdehyde, nitric oxide (NO), D-lactose, and oxidized glutathione (GSSG) concentrations decreased with the increase in dietary Tau (Linear, p < 0.05). The O2•- and •OH clearance rate in serum, liver, and jejunum mucosa increased with the increase in dietary Tau (Linear, p < 0.05). Serum superoxide dismutase (SOD) activity, glutathione peroxidase (GPX) activity, catalase (CAT) activity, and peroxidase (POD) activity and total antioxidant capacity increased with the increase in dietary Tau (Linear, p < 0.05). The serum glutathione (GSH) concentration and the ratio of GSH to GSSG increased with the increase in dietary Tau (Linear, p < 0.05). The POD and glutathione synthase activity in the liver and jejunum mucosa increased with the increase in dietary Tau (Linear, p < 0.05). The mRNA abundances of HO-1 and GPX1 in the H-Tau group were higher than that in the L-Tau, M-Tau, and CON groups (p < 0.05). The mRNA abundances of SOD1 and Nrf2 in the M-Tau and H-Tau groups were higher than in the L-Tau and CON groups (p < 0.05). The mRNA abundance of SOD2 in the L-Tau, M-Tau, and H-Tau groups was higher than in the CON group (p < 0.05). The VH and the ratio of VH to CD of jejunum and ileum increased with the increase in dietary Tau (Linear, p < 0.05). The mRNA abundances of occludens 1 and claudin 1 in the H-Tau group were higher than that in the CON, L-Tau, and M-Tau (p < 0.05). The mRNA abundance of occludin in the L-Tau, M-Tau, and H-Tau groups was higher than that in CON (p < 0.05). The abundance of Firmicutes increased with the increase in dietary Tau (Linear, p < 0.05), while Proteobacteria and Spirochaetota decreased with the increase in dietary Tau (Linear, p < 0.05). Collectively, dietary supplementation of 0.3% and 0.4% Tau in feed could significantly improve the growth performance and enhance the antioxidant capacity of piglets.

Dietary Supplementation of Lactobacillus johnsonii RS-7 Improved Antioxidant and Immune Function of Weaned Piglets.

We investigated the effects of dietary supplementation of lactic acid bacteria on the immune and antioxidant performance of weaned pigs. A total of 128 Duroc × Landrace × Yorkshire piglets weaned on day 28 with an average body weight of 8.95 ± 1.15 kg were selected and randomly divided into four treatment groups according to body weight and sex for a 28-day study. The four dietary treatments were basal diet (CON), and CON with 0.05% (LJ0.05), 0.1% (LJ0.1), and 0.2% (LJ0.2) Lactobacillus johnsonii RS-7, respectively. The lowest feed-to-gain ratio (F:G) was found when LJ0.1 was added to the diet. The addition of compound lactic acid bacteria to the diet increased the concentrations of TP, ALB, IgA, and IgM on day 14 and IgG, IgA, and IgM on day 28 (p < 0.05) in the blood, with trait values greater for pigs fed LJ0.1 than CON pigs (p < 0.05). Concentrations of antioxidants (CAT, T-AOC, MDA, T-SOD, and GSH) in serum, intestinal mucosa, spleen, liver, and pancreas improved. In summary, dietary supplementation of Lactobacillus johnsonii RS-7 improved the antioxidant and immune function of weaned piglets.

The interaction between dietary fiber and gut microbiota, and its effect on pig intestinal health.

Intestinal health is closely associated with overall animal health and performance and, consequently, influences the production efficiency and profit in feed and animal production systems. The gastrointestinal tract (GIT) is the main site of the nutrient digestive process and the largest immune organ in the host, and the gut microbiota colonizing the GIT plays a key role in maintaining intestinal health. Dietary fiber (DF) is a key factor in maintaining normal intestinal function. The biological functioning of DF is mainly achieved by microbial fermentation, which occurs mainly in the distal small and large intestine. Short-chain fatty acids (SCFAs), the main class of microbial fermentation metabolites, are the main energy supply for intestinal cells. SCFAs help to maintain normal intestinal function, induce immunomodulatory effects to prevent inflammation and microbial infection, and are vital for the maintenance of homeostasis. Moreover, because of its distinct characteristics (e.g. solubility), DF is able to alter the composition of the gut microbiota. Therefore, understanding the role that DF plays in modulating gut microbiota, and how it influences intestinal health, is essential. This review gives an overview of DF and its microbial fermentation process, and investigates the effect of DF on the alteration of gut microbiota composition in pigs. The effects of interaction between DF and the gut microbiota, particularly as they relate to SCFA production, on intestinal health are also illustrated.

Mitochondrial micropeptide MOXI promotes fibrotic gene transcription by translocation to the nucleus and bridging N-acetyltransferase 14 with transcription factor c-Jun.

Progressive fibrosis is a hallmark of chronic kidney disease, but we lack effective treatments to halt this destructive process. Micropeptides (peptides of no more than 100 amino acids) encoded by small open reading frames represent a new class of eukaryotic regulators. Here, we describe that the micropeptide regulator of ß-oxidation (MOXI) regulates kidney fibrosis. MOXI expression was found to be up-regulated in human fibrotic kidney disease, and this correlated with the degree of fibrosis and loss of kidney function. MOXI was expressed in the cytoplasm and mitochondria of cultured tubular epithelial cells and translocated to the nucleus upon Transforming Growth Factor-ß1 stimulation. Deletion of Moxi protected mice against fibrosis and inflammation in the folic acid and unilateral ureteral obstruction models. As a potential molecular therapy, treatment with an antisense MOXI oligonucleotide effectively knocked-down MOXI expression and protected against kidney fibrosis in both models. Bimolecular fluorescence complementation identified the enzyme N-acetyltransferase 14 (Nat14) and transcription factor c-Jun as MOXI binding partners. The MOXI/Nat14/c-Jun complex enhances basal and Transforming Growth Factor-ß1 induced collagen I gene promoter activity. Phosphorylation at T49 is required for MOXI nuclear localization and for complex formation with Nat14 and c-Jun. Furthermore, mice with a MoxiT49A point mutation were protected in the models of kidney fibrosis. Thus, our studies demonstrate a key role for the micropeptide MOXI in kidney fibrosis and identify a new function of MOXI in forming a transcriptional complex with Nat14 and c-Jun.

Dietary Complex Probiotic Supplementation Changed the Composition of Intestinal Short-Chain Fatty Acids and Improved the Average Daily Gain of Growing Pigs.

At present, probiotics are being extensively evaluated for their efficacy as an alternative to antibiotics, and their safety in livestock production. In this study, 128 (Duroc, Yorkshire and Landrace) pigs with an average initial body weight of 28.38 ± 0.25 kg were allocated to four dietary treatments in a randomized complete-block design. There were eight pens per treatment, with four pigs per pen (two barrows and two gilts). Dietary treatments included: (1) control diet; (2) control diet + 0.05% complex probiotic; (3) control diet + 0.1% complex probiotic; (4) control diet + 0.2% complex probiotic. During the 28-day experimental period, the feeding of 0.1% complex probiotic in the diet increased body weight and average daily gain (p < 0.05). The addition of complex probiotics decreased total cholesterol and glucose concentrations in the blood (p < 0.01). Acetate concentrations in the blood increased from 0.1% complex probiotic in the diet (p < 0.05), while NH3 and H2S emissions in the feces decreased (p < 0.05) from 0.1% or 0.2% complex probiotic in the diet. In conclusion, dietary complex probiotic supplementation changed the composition of intestinal short-chain fatty acids and improved growth performance for growing pigs.

Reduced Meal Frequency Decreases Fat Deposition and Improves Feed Efficiency of Growing-Finishing Pigs.

An experiment was conducted to examine the effect of meal frequency on growth performance, nutrient digestibility, carcass quality, and lipid metabolism in growing−finishing pigs. Sixty-four Duroc × Landrace × Yorkshire barrows and gilts (26.40 ± 2.10 kg initial body weight) were used in a 112-d experiment in a randomized complete blocked design. The two treatments were the free-access feed group (FA) and the three meals per day group (M3), respectively. The result showed that the average daily feed intake (ADFI) and F: G of the FA group were significantly higher than that in the M3 group during the whole experiment (p < 0.05). Reducing meal frequency also decreased the concentration of triglycerides and urea nitrogen but increased the concentration of insulin and free fatty acids in the blood (p < 0.05). Reducing meal frequency decreased compositions of backfat, belly, and fatty pieces but increased compositions of ham, longissimus muscle, and lean pieces in the carcass (p < 0.05). Greater enzyme activities of ME and FAS and higher mRNA expression of FAS and PPARγ were found in the LM of FA pigs compared with M3 pigs (p < 0.05). In summary, a lower meal frequency improves feed efficiency by regulating lipid metabolism and reducing fat deposition.

Microspectroscopic visualization of how biochar lifts the soil organic carbon ceiling.

The soil carbon (C) saturation concept suggests an upper limit to the storage of soil organic carbon (SOC). It is set by the mechanisms that protect soil organic matter from mineralization. Biochar has the capacity to protect new C, including rhizodeposits and microbial necromass. However, the decadal-scale mechanisms by which biochar influences the molecular diversity, spatial heterogeneity, and temporal changes in SOC persistence, remain unresolved. Here we show that the soil C storage ceiling of a Ferralsol under subtropical pasture was raised by a second application of Eucalyptus saligna biochar 8.2 years after the first application-the first application raised the soil C storage ceiling by 9.3 Mg new C ha-1 and the second application raised this by another 2.3 Mg new C ha-1. Linking direct visual evidence from one-, two-, and three-dimensional analyses with SOC quantification, we found high spatial heterogeneity of C functional groups that resulted in the retention of rhizodeposits and microbial necromass in microaggregates (53-250 µm) and the mineral fraction (<53 µm). Microbial C-use efficiency was concomitantly increased by lowering specific enzyme activities, contributing to the decreased mineralization of native SOC by 18%. We suggest that the SOC ceiling can be lifted using biochar in (sub)tropical grasslands globally.

Identification of novel key genes and potential candidate small molecule drugs in diabetic kidney disease using comprehensive bioinformatics analysis.

Objective: The currently established diagnostic and prognostic tools for diabetic kidney disease (DKD) have limitations, which demands the necessity to find new genes and pathways associated with diagnosis and treatment. Our study aims to reveal the gene expression alteration and discover critical genes involved in the development of DKD, thus providing novel diagnostic molecular markers and therapeutic targets. Materials and methods: The differences of infiltrating immune cells within kidney were compared between healthy living donors and DKD patients. Besides, differentially expressed genes (DEGs) within kidney from healthy living donor, early stage DKD and advanced stage DKD samples were detected. Furthermore, the weighted co-expressed network (WGCNA) and protein-protein interaction (PPI) network were constructed, followed by recognition of core hub genes and module analysis. Receiver operating characteristic (ROC) curve analysis was implemented to determine the diagnostic value of hub genes, correlation analysis was employed to explore the association between hub genes and infiltrating immune cells, and certain hub genes was validated by quantitative real-time PCR and immunohistochemistry staining in cultured tubule cells and diabetic mice kidney. Finally, the candidate small molecules as potential drugs to treat DKD were anticipated through utilizing virtual screening and molecular docking investigation. Results: Our study revealed significantly higher proportion of infiltrating immune cells within kidney from DKD patients via probing the immune landscape by single-cell transcriptomics. Besides, 126 commonly shared DEGs identified among three group samples were enriched in immune biological process. In addition, the ROC curve analysis demonstrated the strong diagnostic accuracy of recognized hub genes (NFKB1, DYRK2, ATAD2, YAP1, and CHD3) from PPI network. Correlation analysis further confirmed the positive association between these hub genes with infiltrating natural killer cells. More importantly, the mRNA transcripts and protein abundance of YAP1 were significantly higher in high glucose-treated renal tubule cells and diabetic mice kidney, and the small molecules exhibiting the best binding affinities with YAP1 were predicted and acquired. Conclusion: Our findings for the first time indicate that NFKB1, DYRK2, ATAD2, YAP1, and CHD3 might be potential novel biomarkers and therapeutic targets for DKD, providing insights into the molecular mechanisms underlying the pathogenesis of DKD.

Synergistic Cr2 O3 @Ag Heterostructure Enhanced Electrocatalytic CO2 Reduction to CO.

The electrocatalytic CO2 RR to produce value-added chemicals and fuels has been recognized as a promising means to reduce the reliance on fossil resources; it is, however, hindered due to the lack of high-performance electrocatalysts. The effectiveness of sculpturing metal/metal oxides (MMO) heterostructures to enhance electrocatalytic performance toward CO2 RR has been well documented, nonetheless, the precise synergistic mechanism of MMO remains elusive. Herein, an in operando electrochemically synthesized Cr2 O3 -Ag heterostructure electrocatalyst (Cr2 O3 @Ag) is reported for efficient electrocatalytic reduction of CO2 to CO. The obtained Cr2 O3 @Ag can readily achieve a superb FECO of 99.6% at -0.8 V (vs RHE) with a high JCO of 19.0 mA cm-2 . These studies also confirm that the operando synthesized Cr2 O3 @Ag possesses high operational stability. Notably, operando Raman spectroscopy studies reveal that the markedly enhanced performance is attributable to the synergistic Cr2 O3 -Ag heterostructure induced stabilization of CO2 •- /*COOH intermediates. DFT calculations unveil that the metallic-Ag-catalyzed CO2 reduction to CO requires a 1.45 eV energy input to proceed, which is 0.93 eV higher than that of the MMO-structured Cr2 O3 @Ag. The exemplified approaches in this work would be adoptable for design and development of high-performance electrocatalysts for other important reactions.

Computational Analysis Reveals the Characteristics of Immune Cells in Glomerular and Tubulointerstitial Compartments in IgA Nephropathy Patients.

Objective: The commonalities and differences regarding immune states between glomerular and tubulointerstitial compartments of IgA nephropathy (IgAN) remains largely undetermined. We aim to perform bioinformatic analysis for providing a comprehensive insight into the characteristics of immune cells and associated molecular mechanisms in IgAN. Materials and Methods: We performed integrated bioinformatic analyses by using IgAN-related datasets from the Gene Expression Omnibus database. First, the differentially expressed genes (DEGs) were identified and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Then, CIBERSORT was employed to determine the landscape of infiltrating immune cells in both glomerular and tubulointerstitial compartments of IgAN patients, followed by Pearson's correlation analysis and principal component analysis (PCA). Finally, commonly shared DEGs between glomerular and tubulointerstitial entities were recognized, followed by correlation analyses to identify the dominant commonly shared DEGs associated with immune cell infiltration in IgAN. Results: GO and KEGG enrichment analyses showed apparently distinct biological processes in the glomerular and tubulointerstitial compartments of IgAN. In addition, CIBERSORT analyses revealed a clear trend of increasing proportions of M1 macrophage and M2 macrophage in the glomerular compartment while noticeably higher proportions of resting CD4+ memory T cells and M2 macrophages in the tubulointerstitial compartments. The PCA analyses showed that the varying composition of immune cells in both glomerular and tubulointerstitial entities was compelling to distinguish IgAN patients from healthy living controls. In addition, 21 commonly shared DEGs between glomerular and tubulointerstitial entities were recognized as key regulators in the pathogenesis of IgAN, among which the enhanced hemoglobin subunit beta (HBB) gene expression was found to be positively associated with M2 macrophage in the glomerular compartment and resting CD4+ memory T cells in the tubulointerstitial compartment. Most importantly, FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene deficiency was recognized as the dominant alteration in promoting M2 macrophage infiltration in the glomerular compartment of IgAN. Conclusion: The findings from our current study for the first time reveal commonalities and differences regarding immune states between glomerular and tubulointerstitial compartments, as well as decode the essential role of M2 macrophages and associated molecular patterns within the microenvironments of IgAN.

Effects of Dietary Zinc Sources on Growth Performance and Gut Health of Weaned Piglets.

The present study aimed to investigate the effects of dietary zinc sources on the growth performance and gut health of weaned piglets. In total, 96 Duroc × Landrace × Yorkshire (DLY) weaned piglets with an initial average body weight of 8.81±0.42kg were divided into four groups, with six replicates per treatment and four pigs per replicate. The dietary treatment groups were as follows: (1) control group, basal diet; (2) zinc sulphate (ZnSO4) group, basal diet +100mg/kg ZnSO4; (3) glycine zinc (Gly-Zn) group, basal diet +100mg/kg Gly-Zn and (4) zinc lactate group, and basal diet +100mg/kg zinc lactate. The whole trial lasted for 28days. Decreased F/G was noted in the Gly-Zn and zinc lactate groups (p<0.05). The zinc lactate group had a lower diarrhea rate than the control group (p<0.05). Moreover, the ZnSO4, Gly-Zn, and zinc lactate groups had significantly higher apparent total tract digestibility of dry matter (DM), crude protein (CP), ether extract (EE), crude ash, and zinc than the control group (p<0.05). The Gly-Zn and zinc lactate groups had higher jejunal villus height and a higher villus height:crypt depth ratio than the control group (p<0.05). In addition, the ZnSO4, Gly-Zn and zinc lactate groups had a significantly lower mRNA expression level of jejunal ZRT/IRT-like protein 4 (ZIP4) and higher mRNA expression level of jejunal interleukin-1ß (IL-1ß) than the control group (p<0.05). The mRNA expression level of jejunal zinc transporter 2 (ZNT2) was higher and that of jejunal Bcl-2-associated X protein (Bax) was lower in the Gly-Zn and zinc lactate groups than in the control group (p<0.05). Moreover, the zinc lactate group had a higher count of Lactobacillus spp. in the cecal digesta and higher mRNA expression levels of jejunal occludin and mucin 2 (MUC2) than the control group (p<0.05). In conclusion, dietary supplementation with 100mg/kg ZnSO4, Gly-Zn, or zinc lactate could improve the growth performance and gut barrier function of weaned piglets. Dietary supplementation with organic zinc, particularly zinc lactate, had the best effect.

Effects of Ellagic Acid Supplementation on Jejunal Morphology, Digestive Enzyme Activities, Antioxidant Capacity, and Microbiota in Mice.

Ellagic acid (EA), a plant polyphenol mainly found in nuts and fruits, exhibits various biological effects. However, the effects of EA on intestinal health remain poorly understood. Hence, the present study aimed to assess the effects of EA supplementation on jejunal morphology, digestive enzyme activities, antioxidant capacity, and microbiota in C57BL/6J mice. A total of 144 mice were randomly assigned to three treatments groups: the control (CON) group received a standard pellet diet, the 0.1% EA group received a standard pellet diet plus 0.1% EA, and the 0.3% EA group received a standard pellet diet plus 0.3% EA. The mice were killed at the end of the experimental period, and jejunal samples were collected. The results revealed that the mice in the 0.3% EA group had higher (P < 0.05) average daily gain and greater (P < 0.05) jejunal villus height than those in the CON group. In addition, the jejunal lactase and sucrase activities were higher (P < 0.05) in the 0.1% EA and 0.3% EA groups, and the alkaline phosphatase activity was higher (P < 0.05) in the 0.3% EA group than in the CON group. Compared with the CON group, the administration of EA increased (P < 0.05) the superoxide dismutase and catalase activities but decreased (P < 0.05) the malonaldehyde content in the jejunum. Moreover, the jejunal messenger RNA expression levels of nuclear factor-E2-related factor 2 (Nrf2) and haem oxygenase-1 (HO-1) were higher (P < 0.05) in the 0.3% EA group than in the CON group. Furthermore, compared with the CON group, the count of Escherichia coli decreased (P < 0.05), and that of Lactobacillus species increased (P < 0.05) in the 0.3% EA group. In general, our findings indicate that the administration of EA can enhance the growth of mice, promote intestinal development, increase the antioxidant capacity, and regulate the intestinal microbiota.

The Effect of Ellagic Acid on Hepatic Lipid Metabolism and Antioxidant Activity in Mice.

Accumulating evidence has demonstrated that the imbalance of lipid metabolism and antioxidant capacity leads to damage to liver. The present study aimed to investigate the effects of ellagic acid (EA), a phenolic compound, on hepatic lipid metabolism and antioxidant activity in mice. In our study, 24 C57BL/6J mice were divided into three groups: (1) control (CON); (2) basal diet+0.1% EA (EA1); and (3) basal diet+0.3% EA (EA2). After the 14-day experiment, the liver was sampled for analysis. The results showed that 0.3% EA administration increased the liver weight. Total cholesterol and low-density lipoprotein cholesterol activities decreased and high-density lipoprotein cholesterol activity increased by EA supplementation. Meanwhile, dietary supplementation with EA dose-dependently decreased the acetyl-CoA carboxylase protein abundance and increased the phospho-hormone-sensitive lipase, carnitine palmitoyltransferase 1B, and peroxisome proliferator-activated receptor alpha protein abundances. Moreover, EA supplementation reduced the malonaldehyde concentration and increased the superoxide dismutase and catalase concentrations. The protein abundances of phospho-nuclear factor-E2-related factor 2, heme oxygenase-1, and NAD(P)H: quinone oxidoreductase 1 increased by EA supplementation in a dose-dependent manner. Taken together, EA supplementation promoted the lipid metabolism and antioxidant capacity to maintain the liver health in mice.

Renoprotective Effect of Oridonin in a Mouse Model of Acute Kidney Injury via Suppression of Macrophage Involved Inflammation.

Ischemia-reperfusion injury (IRI) is the major cause of acute kidney injury (AKI). The previous studies demonstrated that Oridonin can protect kidney against IRI-induced AKI, but the underlying molecular mechanism is unclear. In this study, it showed that Oridonin significantly improved kidney damage, and inhibited the expression of interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α and MCP-1, as well as macrophage marker F4/80 in kidney and the secretion of inflammatory cytokins in serum of AKI mice in vivo. In addition, Oridonin also effectively reduced the expression and secretion of lipopolysaccharide (LPS)-induced inflammatory factors in macrophage cell line RAW264.7 in vitro. Notably, Oridonin strongly downregulated Mincle and AKT/nuclear factor-kappaB (NF-κB) signaling both in vivo and in vitro, and the results of cellular recovery experiments of overexpression of Mincle in macrophage suggested that Oridonin suppressed inflammatory response of macrophage through inhibiting Mincle, which may be the underlying mechanism of Oridonin improving injury in kidney of AKI mice. In summary, the above results indicated that Oridonin can protect kidney from IRI-induced inflammation and injury by inhibiting the expression of Mincle in macrophage.

Infusion of short chain fatty acids in the ileum improves the carcass traits, meat quality and lipid metabolism of growing pigs.

Short chain fatty acids (SCFA) are the main products of indigestible carbohydrates undergoing bacterial fermentation in the hindgut, which are related to some physiological functions. This study was designed to investigate the effects of SCFA infusion by ileum on the carcass traits, meat quality and lipid metabolism of growing pigs. In a 28-day study, 24 growing barrows fitted with a T-cannula in distal ileum were divided into 4 treatments: 1) Control, 2) antibiotics (AB), 3) AB + 300 mL of SCFA1 solution (ABS1), 4) AB + 300 mL of SCFA2 solution (ABS2). The concentrations of acetate, propionate and butyrate in SCFA1 solution were respectively 61.84, 18.62 and 12.55 mmol/L, and in SCFA2 were respectively 40.08, 15.41 and 9.78 mmol/L. The results showed that the SCFA infusion increased the average daily feed intake and average daily gain of pigs (P < 0.05). Meanwhile, the SCFA treatments increased longissimus dorsi area (P < 0.05) and carcass weight (P = 0.058), decreased the drip loss of longissimus dorsi (P = 0.059), and reduced serum concentrations of triglyceride, total cholesterol and urea nitrogen (P < 0.05). Besides, the SCFA administration inhibited the mRNA expressions of fatty acid synthase (FAS) and acetyl-CoA carboxylase in longissimus dorsi (P < 0.05), the mRNA expression of FAS in the liver (P < 0.05), and the mRNA expression of hormone-sensitive lipase in abdominal fat (P < 0.05). Short chain fatty acid infusion also enhanced the mRNA expression of carnitine palmitoyltransferase-1α in the liver (P < 0.05), the mRNA expressions of peroxisome proliferator activated receptor gamma and lipoprotein lipase in abdominal fat (P < 0.05), and the mRNA expressions of free fatty acid receptor 2, glucose-6-phosphatase and phosphoenolpyruvate carboxykinase 1 in the colon (P < 0.05). These results suggested that SCFA administration in the ileum could improve the carcass traits and meat quality of growing pigs, which was possibly due to the fact that SCFA modulated lipid metabolism.

Mg alloy surface immobilised with caerin peptides acquires enhanced antibacterial ability and putatively improved corrosion resistance.

Magnesium (Mg) has mechanical properties similar to human bones and Mg alloy is considered ideal medical implant material. However, the high velocity of degradation inside the human inner environment severely hampers the usage of Mg alloys. In this study, caerin peptide 1.9 (F3) and a modified sequence of caerin 1.1 (F1) with anti-bacterial activity, were covalently immobilised on the surface of Mg alloys by plasma chemical click reaction. The in vitro antibacterial activity and corrosion resistance of these caerin peptide-immobilised Mg alloys were investigated in Dulbecco's Modified Eagle Medium (DMEM) solution. Un-immobilised Mg alloy sample, blank drug-sensitive tablet (BASD) and a commonly used antibiotics Tazocin were used for comparison. Results showed that peptide immobilised Mg samples showed observable improved corrosion resistance and prolonged antibacterial effect compared to non-immobilised Mg alloy and free caerin peptides. These results indicate that coating Mg alloy with caerin peptides obviously increases the alloy's antibacterial ability and putatively improves the corrosion resistance in vitro. The mechanism underlying the prolonged antibacterial effect for annealed Mg alloys immobilised with the peptides (especially F3) remains unclear, which worth further experimental and theoretical investigation.