內(nèi)容: Krill oil (KO) exhibits various biological activities, such as anti-inflammatory and antitumor effects. However, the inhibitory effects of benign prostatic hyperplasia (BPH) in vitro and in vivo have not yet been studied. This study investigated the anti-BPH effects of KO extracted by an enzymatic hydrolysis method. KO treatment inhibited the proliferation of WMPY-1 and BPH-1 cells by induction of G0/G1 phase arrest through the modulation of positive and negative regulators in both prostate cell types. KO treatment stimulated phosphorylation of c-Jun N-terminal kinase (JNK) and p38 signaling. In addition, KO changed the expression of BPH-related markers (5α-reductase, androgen receptor, FGF, Bcl-2, and Bax) and the activity of the proliferation-mediated NF-κB binding motif. KO-induced levels of proliferation-mediated molecules of prostate cells were attenuated in the presence of siRNA-specific p-38 (si-p38) and JNK (si-JNK). Furthermore, the administration of KO alleviated prostate size and weight and the cell layer thickness of prostate glands in a testosterone enanthate-induced BPH rat model. KO treatment altered the level of dihydrotestosterone in serum and the expression levels of BPH-related markers in prostate tissues. Finally, KO-mediated inhibition of prostatic growth was validated by histological analysis. These results suggest that KO has an inhibitory effect on BPH in prostate cells in vitro and in vivo. Thus, KO might be a potential prophylactic or therapeutic agent for patients with BPH.

內(nèi)容: Atherosclerosis (AS) is a major cause of cardiovascular diseases (CVDs) and a strong link with hepatic steatosis. Silver carp muscle hydrolysate (SCH) possess various beneficial activities but its effect on AS and hepatic steatosis is yet unknown. This study aimed to investigate the effects of SCH on AS lesions and hepatic steatosis using apoE-/- mice. Results showed that SCH significantly reduced the vascular AS plaques and alleviated hepatic steatosis lesions in apoE-/- mice. Consistent with this, the lipid levels both in circulation and liver were lowered by SCH. The mechanism analysis showed SCH down-regulated the expression of genes involved in lipoproteins production while up-regulated the expression of genes related to reverse cholesterol transport (RCT) in liver. Meanwhile, SCH remarkably promoted transintestinal cholesterol excretion (TICE) process in intestine, partly contributing to the reduction of blood lipids. The peptide profile data indicated LYF, HWPW, FPK, and YPR are the main peptides in SCH that play a vital role in alleviating AS lesions and hepatic steatosis. Our findings provided new knowledge for the application of SCH in ameliorating CVDs and liver diseases.

內(nèi)容: Inflammatory bowel disease (IBD) is a chronic relapsing-remitting systemic disease of the gastrointestinal tract, characterized by an inflammatory process. Gut mycobiota community dysbiosis has been reported that is closely related to the development of IBD. Our previous findings indicated that polyphenol of the inner shell (BPIS) from foxtail millet bran could restore the gut microbiome and inhibit the progress of colorectal cancer (CRC). In the present study, we studied the anti-inflammatory potential of BPIS in the dextran sodium sulfate (DSS)-induced mouse colitis model. Data suggested that BPIS alleviated experimental colitis by restoring body weight, colonic length and protecting the epithelial architecture from damage by DSS. Moreover, we found that BPIS strengthened the gut barrier function and inhibited the activation of Wnt1/β-catenin pathway. Gene sequence analysis indicated that BPIS remodeled the overall structure of the gut mycobiota from colitis mice toward that of the normal counterparts, including 1 phylum and 9 genera. Interestingly, BPIS significantly increased the abundance of Aspergillus ruber. It further verified that BPIS significantly promoted the growth of A. ruber in vitro. Collectively, BPIS has great potential to develop into an effective against IBD drug.

內(nèi)容: Potentilla anserina L. (PA) belongs to the Rosaceae family, is a common edible plant in the Qinghai-Tibet Plateau areas of China. This study elucidates the mechanism upon which crude polysaccharide of PA (PAP) on fat accumulation in HepG2 cells stimulated by oleic acid (OA) and high fat high sugar induced mice. The result revealed that PAP inhibited lipid accumulation in obese mice and ameliorated the degree of damage in OA-induced HepG2 cells. Specifically, compared to the control group, the TG and TC levels were decreased in cells and mice serum, the aspartate transaminase and alamine aminotransferase contents were declined in liver of obese mice by PAP treatment. The expressions of adipogenic genes of SREBP-1c, C/EBPα, PPARγ, and FAS were inhibited after PAP treatment. Moreover, PAP increased the mRNA levels of CPT-1 and PPARα, which were involved in fatty acid oxidation. The present results indicated the PAP could alleviate the damage of liver associated with obesity and PAP treatment might provide a dietary therapeutic option for the treatment of hyperlipidemia.

內(nèi)容: Crocetin displays strong antioxidant, anti-inflammatory and anti-depression activity which is promising to relieve symptoms of fatigue. As a carotenoid, crocetin is difficult to dissolve in water and highly unstable against many environmental factors. Nanoliposome is used to encapsulate crocetin to improve its water dispersion. In the present study, the antifatigue activities and potential mechanism of crocetin loaded nanoliposome (CLN) was extensively investigated. The potential antifatigue pathway of CLN was analyzed. Furthermore, impact of CLN on the gut microbiota structure was examined which contributes to its antifatigue functions. CLN significantly increases exhaustive swimming time of fatigue mice, decreases the blood contents of lactic, blood urea nitrogen (BUN) and malondialdehyde (MDA). At the same time, CLN improves the activity of glutathione peroxidase (GSH-Px) and succinate dehydrogenase (SDH) enzyme, attenuates the oxidant stress in mice. CLN activates the adenosine monophosphate-activated kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) signaling pathway of fatigue mice, increases the mRNA expression of ATP synthase. It also increases mRNA expression of mitochondrial transcription factor A (TFAM) which promotes mitochondrial biogenesis. Additionally, CLN ameliorates the gut microbiota structure by increasing the abundance of genus such as Lactobacillus in fatigue mice. In summary, CLN exerts strong anti-fatigue properties by decreasing the oxidant stress and the contents of harmful metabolites, augmenting the production of ATP, and potentially ameliorating the gut microbiota structure.

內(nèi)容: Plant protein beverage adulteration occurs frequently, which may cause health problems for consumers due to the hidden allergens. Hence, a novel method was developed for authentication by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Almond, peanut, walnut and soybean were hydrolyzed, followed by separation by NanoLC-Triple TOF MS. The obtained fingerprints were identified by ProteinPilotTM combined with Uniprot, and 16 signature peptides were selected. Afterwards, plant protein beverages treated by trypsin hydrolysis were analyzed with UPLC-MS/MS. This method showed a good linear relationship with R2 > 0.994 03. The limit of quantification (LOQ) were 0.015, 0.01, 0.5 and 0.05 g/L for almond, peanut, walnut and soybean, respectively. Mean recoveries ranged from 84.77% to 110.44% with RSDs < 15%. The developed method was successfully applied to the adulteration detection of 31 plant protein beverages to reveal adulteration and false labeling. Conclusively, this method could provide technical support for authentication of plant protein beverages to protect the rights and health of consumers.

內(nèi)容: The protective role of (poly)phenols against metabolic disorders has been extensively studied in adults but not in adolescents. To assess associations of dietary (poly)phenols and their subclasses with cardiometabolic health parameters in adolescents. A cross-sectional study was conducted in 944 individuals aged 11–14 years enrolled in the SI! Program for Secondary Schools trial (NCT03504059). (Poly)phenol intake was assessed using semi-quantitative food frequency questionnaires and the Phenol-Explorer database. The measured cardiometabolic parameters were waist circumference (WC) age-sex Z-score, blood pressure (BP) age-sex Z-score, blood glucose (BG), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-c). Multilevel mixed-effect linear regression models were applied to examine the association between (poly)phenol quintiles and cardiometabolic health parameters. Compared to the lowest quintile, adolescents in the highest quintile of total (poly)phenol intake had lower WC Z-scores, mean arterial pressure Z-scores, and HDL-c after multivariable adjustment. The WC Z-scores and HDL-c were lower in the highest quintile of flavonoid intake compared to the lowest quintile. The highest quintile of phenolic acid intake was associated with a lower WC Z-score and TG levels, and the highest quintile of stilbene intake with lower BG and TG, and with higher HDL-c compared to the lowest quintile. A higher intake of (poly)phenols, especially flavonoids, phenolic acids, and stilbenes, was associated with better cardiometabolic parameters in adolescents.

內(nèi)容: Selenopeptides may be a valuable bioactive compound to promote gut microbiota-targeted therapeutic methods for intestinal disease and hepatopathy. However, limited information is available on the utilization of selenopeptides by gut microbiota, especially Selenium (Se) function. For this purpose, the present study aimed to investigate the protective effect of selenopeptide (RYNA(Se)MNDYT, Se-P2, purity of ≥ 95%) and its original peptide (RYNAMNDYT, P2, purity of ≥ 95%) in vivo by the microbiota-metabolite axis and further analyze the potential contribution of Se biofortification to Se-P2 bioactivity. The results showed that Se-P2 exhibits a higher protective effect on lipopolysaccharide (LPS)-induced inflammation than P2, including pathology of the colon and liver, which suggested that the bioactivity of P2 was promoted by the organic combination of Se. Notably, gut microbiota composition tended to be a healthy structure by Se-P2 pretreatment in LPS-injured mice, which had a positive effect on LPS-induced gut microbiota dysbacteriosis. Additionally, only Se-P2 promoted an increase in the relative abundance of Lactobacillus, Alistipes, and Roseburia and a decrease in the relative abundance of Akkermansia, Erysipelatoclostridium, and Bacteroides in LPS-injured mice. The changes in gut microbiota were obviously correlated with the changes in metabolites and affected the metabolic pathways of valine, leucine, isoleucine, phenylalanine, tyrosine, and tryptophan biosynthesis and phenylalanine metabolism. This may be one of the key reasons for Se-P2 to exert bioactivity through the microbiota-metabolite axis. Furthermore, Se-biofortification in Se-enriched Cordyceps militaris affected the parental proteins of Se-P2 to modulate mitogen-activated protein kinase, GPI anchored protein, and carbohydrate metabolism, translation, folding, sorting and degradation, which may contribute to the bioactivity of Se-P2. Our study provides information on the effect of Se on selenopeptides in vivo, which further promotes the prospective applications of selenopeptides as dietary supplements.

內(nèi)容: Gut microbiota plays a crucial role in the pathophysiology of depression. This study aimed to explore the antidepressant effect of mature whole Citrus aurantium fruit extract (FEMC) in the chronic unpredictable mild stress (CUMS) model. The behavioral tests were applied to assess antidepressant effect and 16S rRNA sequencing was used to analyze the changes of gut microbiota. The results showed that the major components of FEMC were naringin and neohesperidin and significantly increased the sucrose preference index of the mice. FEMC also could reduce the feeding latency in an open field test and the rest time in a novelty suppressed feeding test. In addition, FEMC could increase CUMS-induced reduction in the levels of BDNF, PSD95, and SYN in the hippocampus. Moreover, FEMC intervention slightly decreased the ratio of Firmicutes to Bacteroidota. Meanwhile, FEMC reduced the abundance of the Prevotellaceae_Ga6A1_group, [Ruminococcus]_torques_group, which have been reported to be closely related to inflammation. Bioinformatics analysis revealed that mitogen-activated protein kinase (MAPK) signaling pathway and lipopolysaccharide biosynthesis were involved in the anti-inflammatory effect of FEMC in the CUMS animal model. Finally, the ELISA results showed that FEMC could significantly reduce the expression of pro-inflammatory cytokines IL-6 and TNF-α in the serum of depressive mice. Our results suggest FEMC can ameliorate depressive behavior by inhibiting gut microbiota-mediated inflammation in mice.

內(nèi)容: To explore the oxidation mechanism of wooden breast myofibrillar protein (WBMP), oxidative breast MP (OBMP) was obtained from different doses (3, 10, and 20 mmol/L) of H2O2 oxidized normal breast MP (NBMP). The results showed that the Zeta-potential, particle size, solubility, sulfhydryl, and carbonyl contents of OBMP-3 (3 mmol/L, low-dose free radicals) and WBMP were similar. Fluorescence spectrum analysis showed that the oxidation of low-dose free radicals led to a significant increase in the surface hydrophobicity (from 214.03 ± 10.03 to 393.50 ± 10.33) and tryptophan fluorescence intensity (from 185.71 to 568.32). In addition, the α-helix content of WBMP decreased significantly from (37.46 ± 1.15)% (NBMP) to (34.70 ± 2.04)%, while β-sheet and random coil contents increased significantly (P < 0.05) from (14.37 ± 0.69)% and (22.24 ± 0.78)% (NBMP) to (17.70 ± 0.87)% and (25.20 ± 1.47)% (WBMP). In summary, low-dose free radical oxidation attacks protein groups, inducing secondary and tertiary structural changes, leading to the formation of WBMP. This work will provide a theoretical basis at the molecular level for exploring the mechanism of functional degradation of WBMP.