內(nèi)容: Obesity is associated with skeletal muscle mass loss and physical dysfunction. Krill oil (KO) has been shown to be beneficial in human health. However, the effect of KO on obesity-induced skeletal muscle atrophy is still unclear. In this study, the male C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity, and then were intragastric administration with 400 mg/kg bw KO for an additional 6 weeks. The results showed that KO treatment reduced body weight, fat accumulation and serum pro-inflammatory cytokines in HFD-induced obese mice. Importantly, KO treatment attenuated skeletal muscle atrophy in HFD-fed mice, as evidenced by preserving skeletal muscle mass, average myofiber cross-sectional area and grip strength. KO administration also mitigated obesity-induced ectopic lipid deposition and inflammatory response in skeletal muscle. Additionally, KO treatment inhibited the transcriptional activities of nuclear factor-κB (NF-κB) p65 and forkhead box O 3a (FoxO3a), and then down-regulated muscle atrophy F-box (MAFbx) and muscle-specific RING finger protein 1 (MuRF1) protein levels in skeletal muscle from HFD-fed mice. KO administration also improved obesity-induced impaired muscle protein synthesis via activating PI3K/Akt pathway. Furthermore, KO treatment enhanced muscle mitochondrial biogenesis in HFD-induced obese mice via activating PGC-1α pathway. Collectively, KO might be developed as a potential nutritional supplement for the prevention and treatment of obesity-induced skeletal muscle atrophy.

內(nèi)容: Chronic kidney disease (CKD) is one kind of illness with abnormal renal structure and function caused by many factors. Probiotics can be used to regulate intestinal microflora and enhance intestinal mucosal barrier, thus, intervention with probiotics may be regarded as one of the potential ways to protect against CKD. In vitro and in vivo experiments showed that Lactiplantibacillus plantarum MA2 (MA2), a probiotic separated from traditional Chinese Tibetan kefir grains, could degrade the uremic toxins including creatinine, urea nitrogen and uric acid. Oral administration of MA2 or its inactive strains (IMA2) could decrease serum uremic toxins of adenine-induced CKD mice, and also elevate the relative expression of claudin-1. Meanwhile, intervention of MA2 or IMA2 decreased the contents of lipopolysaccharide, Toll-like receptor 4 (TLR4) and interleukin-1β (IL-1β) in the kidney. 16S rDNA sequencing results indicated that the intervention of MA2 or IMA2 regulated the gut microbiota structure by elevating the abundance of Lactobacillus, and decreasing the abundance of Proteobacteria. Thus, oral administration of MA2 or IMA2 can reduce the uremic toxins in CKD mice by regulating gut microflora and restoring the intestinal mucosal barrier. Our study provided a theoretical basis for the application of MA2 and its postbiotics in the CKD intervention and treatment.

內(nèi)容: The present study monitored bacterial succession, physicochemical properties, and volatile organic compounds (VOCs) changes in smoked chicken legs with modified atmosphere packaging (MAP, 60% CO2 and 40% N2) during a 25-day storage period at 4 °C. After 15 days of storage, Serratia proteamaculans and Pseudomonas fragi became the predominant bacteria. Furthermore, physicochemical properties changed significantly, as evidenced by an increase in thiobarbituric acid reactive substances and b* (yellowness) value, and a decrease in hardness. A total of 65 VOCs were identified during storage. Correlation between bacterial succession and quality indicators (including VOCs and physicochemical properties) allowed the identification of 26 core dominant bacteria, including S. proteamaculans, Psychrobacter alimentarius, Pseudomonas putida, and Pseudomonas poae, which were positively related to spoilage VOCs (e.g., 1-octen-3-ol, 1-pentanol, and 3-methyl-1-butanol) and could be defined as specific spoilage organisms (SSOs). The results of this study provide a systematic approach to predict SSOs in smoked chicken legs during storage, which can also provide a basis for product safety.

內(nèi)容: 2’-Fucosyllactose (2’-FL) shows the potential to support intestinal health as a natural prebiotic that bridges the gap between infant formula feeding and breastfeeding. However, the effect and mechanism of 2’-FL in improving intestinal permeability are not clear. In this study, we constructed human microbiota-associated (HMA) mouse models by colonizing healthy infant feces in mice with antibiotic-depleted intestinal microbiota. The protective effect of 2’-FL on the intestinal permeability was explored using the HMA mouse models, and the combination of metagenomics was used to analyze the possible mechanisms by which the microorganisms reduced the intestinal permeability. The results showed that 2’-FL decreased the concentration of markers of intestinal permeability (enterotoxin and diamine oxidase (DAO)) and increased the expression levels of tight junctions (occludin and claudin). Metagenomics revealed the enrichment of Bifidobacterium and increased the expression of glycoside hydrolases (GHs), including GH31, GH28, and GH5. In conclusion, 2’-FL strengthened intestinal permeability function by improving microbiota composition to control the translocation of harmful substance.

內(nèi)容: The surface macromolecules of probiotic bacteria play crucial roles in modulating immune responses in the host. Exopolysaccharide (EPS) from lactic acid bacteria (LAB) have been widely reported to exhibit immunomodulatory activity. In this study, the EPS biosynthesis gene cluster of Lacticaseibacillus paracasei S-NB was analyzed and a deletion mutant S-NBΔ7576 (two genes S-NB_2175/wze and S-NB_2176/wzd were responsible for the chain length determination and export of EPS) was successfully constructed, resulting a 40.02% decrease in the production of EPS. The deletion of wze and wzd had little effect on the monosaccharide composition and major groups of the two EPS fractions (BEPS1 and BEPS2). Both BEPS1 and BEPS2 could inhibit the transcriptional level of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA in RAW 264.7 cells induced by lipopolysaccharide (LPS), and enhance host immune tolerance via suppressing NF-κB and MAPK signaling. Notably, the S-NBΔ7576 mutant supplied with the BEPS1/BEPS2 exhibited more significant inhibition of cytokines production and the phosphorylation of p65 and c-Jun N-terminal kinase (JNK) in LPS-stimulated cells compared with the S-NBΔ7576 mutant alone. Our study provided the immunomodulatory effect of BEPS1 and BEPS2 from L. paracasei S-NB, in which the wze and wzd genes associated with EPS biosynthesis may play an important role.

內(nèi)容: This study endeavors to investigate the effects of Bifidobacterium breve CCFM1078 on bone formation and resorption balance in growing BALB/c mice. Newborn BALB/c mice were assigned to the control group (administration saline) and the CCFM1078 group (administration B. breve CCFM1078, 3 × 109 CFU/day) in 3-, 4-, and 5-week tests. All the groups have male and female distinctions. Our findings demonstrate that B. breve CCFM1078 exerts on the dynamic equilibrium between bone formation and resorption during the critical period of growth in mice by modulating the composition of gut microbiota and metabolites (hexadecanamide, linoleoyl ethanolamide, and palmitoyl ethanolamide), the genes and proteins expression related to the growth hormone (GH)/insulin-like growth factors-1 (IGF-1) axis and Gs/PKA/CREB signaling pathways, as well as downstream osteogenic and osteoclastic differentiation factors. The effects of B. breve CCFM1078 were different with age and gender dependent. This finding suggests B. breve CCFM1078 may have potential applications in regulating bone metabolism in the growth period population.

內(nèi)容: Anthocyanin, as a typical food bioactive molecule, is capable of reversing inflammatory, oxidative and allergic condition thus contributes to intestinal health. We were wondering whether anthocyanin has influence on the infiltration of inflammatory cells into the intestinal mucosa and thus help enhancing intestinal barrier which could be damaged in some metabolic diseases. In this study, the influence of anthocyanin (administered orally) on the alterations (including structure and permeability) of the intestinal mucosa in mice in response to a high fat-high cholesterol (HFHC) diet was investigated. Primary T helper 17 (Th17) cells were isolated from mouse intestine tissues to observe the modulatory role of anthocyanin through the transcription phosphorylated STAT3 (p-STAT3). The results indicated that anthocyanin significantly alleviated HFHC-induced impairment in the intestinal structures and permeability in a dose-dependent manner; moreover, anthocyanin appeared to inhibit HFHC induced the expression of p-STAT3, thereby disturbing Th17 cell differentiation. In high-fat diet (HFD, cholesterol level non-modified)-challenged mice selective p-STAT3 inhibitor significantly reversed the effects of anthocyanin, which were decreased amount of interleukin (IL)-17A (produced and released from Th17 cells) and the protected intestinal structure/function. In summary, the results of this study suggest that anthocyanin may attenuate the damage of intestinal barrier in HFHC mice through regulating intestinal STAT3-Th17-IL-17A signal transduction pathway.

內(nèi)容: Bifidobacterium longum subsp. infantis is a commensal bacterium that predominates in the infant gut, playing a critical role in both preventing foreign infections and facilitating immune development. This study aimed to explore the effects of B. longum subsp. infantis supplementation on interferon-beta (IFN-β) secretion and intestinal barrier improvement in growing mice. Female and male mice were orally administered either saline or B. longum subsp. infantis CCFM1269 or I5TI (1 × 109 CFU/mice per day, n = 8) from 1-week-age until 3-, 4-, and 5-week-age. RNA sequencing analysis revealed that CCFM1269 exhibited potential antiviral capacity through increasing 2’-5’ oligoadenylate synthetase (OAS). Additionally, CCFM1269 supplementation significantly increased colonic IFN-β levels which combined with OAS in 3-week-old female and male mice by activating the TLR4-TRIF-dependent signaling pathway. However, this effect was not observed in 4- and 5-week-old mice. Furthermore, both CCFM1269 were found to modulate the gut microbiota composition and enhance the intestinal barrier function in 3-, 4-, and 5-week-old mice. In summary, the results of this study suggested that B. longum subsp. infantis CCFM1269 promoting intestinal barrier and releasing IFN-β in growing mice was in a strain-specific and time-dependent manner.

內(nèi)容: Marine fauna provides a plentiful repository of peptides and bioactive proteins. Peptides and proteins isolated from marine animals have been studied and applied in the development of food supplements, drugs, and cosmeceutical products because of their special bioactivities, such as anti-inflammatory and antioxidant effects. This study focused on exploring the alleviating effects of five major marine animal-derived peptides (Apostichopus japonicus, Acaudina leucoprocta, Melanogrammus aeglefinus, Phascolosoma esculenta and Rhopilema esculentum) on adjuvant-induced arthritis (AIA). The treatment with five marine animals-derived peptides downregulated the expression levels of pro-inflammatory cytokines of interleukin (IL)-1β, IL-17 and tumor necrosis factor (TNF)-α in the bones of the mice with AIA and alleviated the rough surface of bone tissues significantly. A. japonicus-treatment ameliorates inflammation by restoring nuclear factor-κB pathway in AIA mice. High-throughput sequencing of the gut microbiota based on 16S rRNA sequencing revealed that A. japonicus peptide-treated AIA mice showed alterations and imbalance of intestinal flora and an increased abundance of Lactobacillus and Clostridium. Furthermore, metabolomic analysis showed that the level of short-chain fatty acids (SCFAs) in the feces was enhanced to different degrees in mice treated with five major marine animal-derived peptides. Taken together, we propose that major marine animal-derived peptides can alleviate arthritis by improving the imbalance in the gut flora and increasing SCFAs production to varying degrees.

內(nèi)容: Selenium is a crucial trace element that contributes to physiological processes in the body as selenoproteins. Selenoproteins serve as an integral role in the body in controlling the redox state of cells and protecting against damage induced by oxidative stress. This study aimed to investigate the effects and possible mechanism of selenium on selenoproteins expression in EA.hy926 cells induced by oxidized low density lipoprotein (oxLDL). The impact of selenium on the viability of EA.hy926 cells was detected by the methylthiazolyldiphenyl-tetrazolium bromide (MTT) method, and intracellular reactive oxygen species (ROS) level and mitochondrial membrane potential were assessed by fluorescent probe DCFH-DA and JC-1, respectively. RNA-seq, quantitative real-time polymerase chain reaction (qPCR), and Western blot were used to investigate the selenoprotein expression. Selenoprotein mRNA translation efficiency was analyzed by ribosome profiling (Ribo-Seq) coupled with transcriptomics. Our data showed that selenium supplementation (0.5 μmol/L) significantly decreased ROS production, increased mitochondrial inner membrane potential and increased the proliferative activity of EA.hy926 cells induced by oxLDL. Moreover, The protective effects of selenium against oxLDL-induced EA.hy926 cell injury were associated with the upregulation of the expressions of selenoproteins glutathione peroxidase 1 (GPX1), glutathione peroxidase 4 (GPX4), and thioredoxin reductase 1 (TXNRD1). Furthermore, the expressions of selenoproteins GPX1 and GPX4 were hierarchically controlled, but the expressions of selenoproteins TXNRD1 were mainly regulated by oxLDL. Finally, Ribo-Seq coupled with transcriptomics results demonstrated that the expressions of selenoproteins GPX1, GPX4, and TXNRD1 were regulated at the translation process level. These findings suggested that selenium could have preventive effects in oxLDL induced EA.hy926 cell injury by regulating the selenoprotein expression, and the selenoproteins expressions at the translation level in vascular endothelial cells need further study.