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Evaluation for biological impact of food emulsions is fundamental for their application. In present study, we utilized a NaCas-DGMO (sodium caseinate-decylglycerol monooleate) stabilized emulsion to improve resveratrol's (Res) stability, and bioavailability. The in vivo interaction between complex emulsion and gut microbiota was further explored. Results indicated NaCas-DGMO emulsion achieved a loading rate of 92 % for Res and significantly enhanced storage and photo stability of Res. In vitro gastrointestinal digestion highlighted a significant improvement in Res's bioaccessibility. In vivo pharmacokinetic tests showed a notable 3.1-fold increase in oral bioavailability, with a prolonged Tmax of 6 h post-administration. Gut microbiota analysis revealed that the emulsion promoted beneficial bacteria, like Blautia, which produce short-chain fatty acids. Consequently, the findings proved potential of NaCas-DGMO stabled emulsion as carriers for bioactive substances in the food industry. The innovative methodology employed in assessing biological effects provides valuable insights for future research in related field.

Soybean-derived phosphatidylethanolamine (PE) is a valuable phospholipid component yet its high-purity form is costly and its molecular structure is poorly understood. The present study combined solvent extraction and cryopurification to purify PE. The optimal extraction conditions were as follows: material-liquid ratio 1:15 (g/mL), ethanol base concentration 100:4 (Vanhydrous ethanol /V25% ammonia), extraction temperature 40 °C, time 60 min, extraction twice. The cryopurification conditions were: material-liquid ratio 1:60, ethanol base concentration 100:6 (Vanhydrous ethanol/V25% ammonia), freezing temperature − 20 °C, time 20 h. UPLC-QTOF-MS/MS analysis revealed phospholipid composition of raw material, crude product, and purified product. The results showed that the purity of PE in the purified products was 76.74%, and the yield was 72.43% under optimal conditions. 181 phospholipid molecules were quantified. The study successfully explored high-purity PE preparation method and the composition of PE product. It provides a basis for the subsequent exploration of its biofunction and potential applications.

1-O-alkylglycerols are a class of natural existing lipids with broad biological activities. However, their use in food or agricultural fields remains to be investigated, especially for their antimicrobial activity. In this work, three 1-O-alkylglycerols, 1-O-octanylglycerol (C8Gly1), 1-O-dodecylglycerol (C12Gly1), and 1-O-hexadecylglycerol (C16Gly1), were synthesized in the isolated yields of 71.3–89.8 % and characterized by 1H NMR, 13C NMR, FITR, mass spectra, and HPLC-ESLD. The critical micelle concentration (CMC) of 1-O-alkylglycerols was determined to be 1.65 mmol/L (C8Gly1), 0.33 mmol/L (C12Gly1), and 0.23 mmol/L (C16Gly1) using the pyrene method. C12Gly1 and C16Gly1 had similar surface tensions that are lower than C8Gly1. C8Gly1 can form micelles in aqueous solution with excellent nano-dispersed uniformity and stability. Furthermore, C8Gly1 and C12Gly1 not only displayed good antibacterial activity against Staphylococcus aureus, but they also inhibited the growth of Botryosphaeria dothidea, Monilia fructigena, and Phytophthora capsicum at 400 μg/mL. Thus, the C8Gly1 and C12Gly1 can serve as novel antimicrobial agents in food preservation.

Four novel nonionic 1-alkylaminoglycerol Gemini surfactants, represented by m-s-m (m = C8 and C12, s = 3 and 4), were synthesized through a two-step reaction in high yields, and confirmed by 1H NMR, 13C NMR, and HRMS. The synthesized Gemini surfactants exhibited low CMC (1.41–5.25 mmol/L), excellent surface-tension-reducing ability (25.45–26.83 mN/m), and wetting ability on hydrophobic interface. Gemini surfactants in aqueous solutions were in stable nanoscale dispersion, and exhibited strong and long-lasting foaming ability and emulsifying abilities for benzene/water and triacylglyceride/water systems. Especially, 12–4-12 solution displayed excellent tolerance to wide pH range and high salinity. Biological evaluation demonstrated that these Gemini surfactants, except for 8–4-8, showed significant antibacterial activities against Staphylococcus aureus and Escherichia coli at 25 and 50 µg/mL. Hence, these Gemini surfactants have the potential to be used in a varieties of fields as highly efficient agents.

Ferric citrate (FC) has been used as an iron fortifier and nutritional supplement, which is reported to induce colitis in rats, however the underlying mechanism remains to be elucidated. We performed a 16-week study of FC in male healthy C57BL/6 mice (nine-month-old) with oral administration of Ctr (0.9 % NaCl), 1.25 % FC (71 mg/kg/bw), 2.5 % FC (143 mg/kg/bw) and 5 % FC (286 mg/kg/bw). FC-exposure resulted in colon iron accumulation, histological alteration and reduce antioxidant enzyme activities, such as glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC), together with enhanced lipid peroxidation level, including malondialdehyde (MDA) level and 4-Hydroxynonenal (4-HNE) protein expression. Exposure to FC was associated with upregulated levels of the interleukin (IL)− 6, IL-1β, IL-18, IL-8 and tumor necrosis factor α (TNF-α), while down-regulated levels of IL-4 and IL-10. Exposure to FC was positively associated with the mRNA and protein expressions of cysteine-aspartic proteases (Caspase)− 9, Caspase-3, Bcl-2-associated X protein (Bax), while negatively associated with B-cell lymphoma 2 (Bcl2) in mitochondrial apoptosis signaling pathway. FC-exposure changed the diversity and composition of gut microbes. Additionally, the serum lipopolysaccharide (LPS) contents increased in FC-exposed groups when compared with the control group, while the expression of colonic tight junction proteins (TJPs), such as Claudin-1 and Occludin were decreased. These findings indicate that the colonic mucosal injury induced by FC-exposure are associated with oxidative stress generation, inflammation response and cell apoptosis, as well as the changes in gut microbes diversity and composition.

Duck-origin parvovirus disease is an epidemic disease mainly caused by duck-origin goose parvovirus (D-GPV), which is characterized by beak atrophy and dwarfism syndrome. Its main symptoms are persistent diarrhea, skeletal dysplasia, and growth retardation. However, the pathogenesis of Cherry Valley ducks infected by D-GPV has not been studied thoroughly. To perceive the distribution of D-GPV in the intestinal tract, intestinal morphological development, intestinal permeability, inflammatory cytokines in Cherry Valley ducks, and expression of tight junction protein, the D-GPV infection was given intramuscularly. Illumina MiSeq sequencing technology was used to analyze the diversity and structure of ileum flora and content of short-chain fatty acids of its metabolites. To investigate the relationship between intestinal flora changes and intestinal barrier function after D-GPV infection on Cherry Valley ducks is of great theoretical and practical significance for further understanding the pathogenesis of D-GPV and the structure of intestinal flora in ducks. The results showed that D-GPV infection was accompanied by intestinal inflammation and barrier dysfunction. At this time, the decrease of a large number of beneficial bacteria and the content of short-chain fatty acids in intestinal flora led to the weakening of colonization resistance of the intestinal flora and the accumulation of potentially pathogenic bacteria, which would aggravate the negative effect of D-GPV damage to the intestinal tract. Furthermore, a significant increase in Unclassified_S24-7 and decrease in Streptococcus was observed in D-GPV persistent, indicating the disruption in the structure of gut microbiota. Notably, the shift of microbiota was associated with the transcription of tight-junction protein and immune-associated cytokines. These results indicate that altered ileum microbiota, intestinal barrier, and immune dysfunction are associated with D-GPV infection. Therefore, there is a relationship between the intestinal barrier dysfunction and dysbiosis caused by D-GPV, but the specific mechanism needs to be further explored.