The rational design of plant protein–phospholipid composite interfacial structures offers a promising strategy for stabilizing and delivering hydrophobic nutrients in emulsion-based food systems. In this study, flaxseed oil–in–water emulsions co-stabilized by sunflower protein isolate (SPI) and phospholipids (PL) at varying ratios were systematically engineered to elucidate their structure–function–digestion relationships. Multispectral characterization revealed that SPI–PL interactions induced distinct protein conformational rearrangements, manifested by a reduction in α-helix content (from 27% to 11%) and a marked increase in surface hydrophobicity. At the oil–water interface, specific SPI/PL ratios (notably 1:1 and 1:3) promoted the formation of viscoelastic, deformation-resistant composite interfacial films with enhanced mechanical strength. These optimized interfacial architectures resulted in the formation of considerably finer emulsion droplets (0.24–0.44 μm, compared with ∼8.0 μm for SPI-only emulsions) and significantly improved physical stability. During in vitro gastrointestinal digestion, PL-enriched emulsions (SPI/PL ratios of 1:3–1:7) exhibited superior gastric stability and accelerated intestinal lipolysis, achieving a peak free fatty acid (FFA) release of 81.8%, compared with 59.1% for the SPI-only emulsion. Importantly, at these ratios, enhanced mixed-micelle formation and greater lipid-loading capacity led to the highest absolute bioaccessibility of α-linolenic acid (approximately 1.35 mg/g). Overall, this study demonstrates that ratio-dependent SPI–PL synergism allows for effective regulation of interfacial architecture, thereby providing an effective strategy for improving the stability, digestibility, and bioaccessibility of bioactive lipids in sustainable, plant-based emulsion delivery systems.

Walnut oil (WO) is rich in polyunsaturated fatty acids, particularly α-linolenic acid, and various bioactive compounds including phenolics, phytosterols, tocopherols, squalene and melatonin, contributing to its broad health benefits. The present study examined whether WO could attenuate cognitive deficits in D-galactose (D-gal)-induced aging mice. Cognitive performance was evaluated by the Morris water maze and step-through passive avoidance tests. WO significantly reversed the cognitive impairments in D-gal-treated mice, as evidenced by shorted the escape latency and swimming distance in the Morris water maze and by prolonged step-through latency with fewer errors in the passive avoidance test. Mechanistically, WO alleviated hippocampal neuronal injury as confirmed by Nissl staining, elevated hippocampal cAMP responsive element binding protein (CREB) activity and brain-derived neurotrophic factor (BDNF) expression, and restored postsynaptic density protein-95 (PSD95) levels, thereby facilitating synaptic plasticity. These findings indicate that WO protects mice against D-gal-induced cognitive decline and may represent a nutritional strategy for mitigating aging-associated cognitive dysfunction.

Flax lignans enhance the metabolic conversion of ALA to n-3 LCPUFAs via structure-specific metabolic routes and metabolite uptake, modulating key processes such as ALA absorption, transport, and hepatic metabolism.

Background Phenethyl isothiocyanate (PEITC) is an isothiocyanate produced from the glucosinolate gluconasturtiin in cruciferous plants and has been shown to reduce fat accumulation. Hypothalamic leptin resistance is a key contributor to obesity. Purpose This study aimed to determine whether PEITC affects hypothalamic leptin signaling and obesity in mice fed a high-fat diet (HFD). Methods Male C57BL/6J mice were randomly divided into four groups. Mice in the control, HFD, low-dose PEITC, and high-dose PEITC groups received a standard diet (10 kcal% fat), HFD (60 kcal% fat), or PEITC-enriched HFD (60 kcal% fat with 0.5‰ or 1‰ PEITC, w/w) for 12 weeks, respectively. Obesity was evaluated by body weight and visceral fat. Leptin signaling, neuroinflammation, endoplasmic reticulum (ER) stress, neuronal activity in hypothalamus, as well as leptin sensitivity were tested. Results PEITC dose-dependently decreased body weight gain and visceral fat in HFD-fed mice. It restored leptin sensitivity and hypothalamic leptin signaling by increasing Ob-Rb expression and JAK2 and STAT3 phosphorylation, while rebalancing leptin signaling regulators. PEITC suppressed hypothalamic neuroinflammation and attenuated ER stress across all three unfolded protein response branches. As a result, PEITC reactivated POMC neurons and inhibited AgRP neurons, enhancing energy metabolism. Conclusion PEITC protects against high-fat diet-induced obesity by improving hypothalamic leptin sensitivity.

This study maps the knowledge structure of walnut protein peptide research (2012-2025) through a bibliometric analysis of 229 publications retrieved from the Web of Science Core Collection, using tools such as Bibliometrix, VOSviewer, and CiteSpace. The results show that there is a clear publication output increase trend. China is the major contributor, South China University of Technology ranks as the top research institution, Journal of Agricultural and Food Chemistry is the core journal, and Min WH and Wang SG are the most cited authors. Furthermore, based on the most cited articles, the study finds research hotspots in the extraction of antioxidant and neuroprotective peptides, bioavailability and absorption mechanisms, and structure-activity relationships, which can be used to promote the research of walnut protein peptide and the development of walnut meal industry.

Traditional Chinese medicine has long regarded flaxseed as a natural remedy for constipation. However, the efficacy or mechanism of flaxseed plant milk (FPM), a functional beverage derived from flaxseed, in alleviating constipation has not yet been clearly established. In this study, network pharmacology was combined with in vivo experiments to evaluate the anti-constipation activity of FPM on water restriction-induced constipation mouse model. Compared with the model group, administration of FPM (100 mg/kg and 200 mg/kg) significantly shortened the time to first black stool excretion, increased number of fecal pellets and water content of fecal pellets, and improved Small Intestinal Transit Rate (p < 0.05). Histological analysis revealed that FPM (200 mg/kg) preserved colonic epithelial integrity, reduced lamina propria damage, and restored goblet cell populations. Serum biochemical assays showed that FPM decreased vasoactive intestinal peptide (VIP) levels and increased 5-hydroxytryptamine (5-HT) concentrations. Network pharmacology identified 214 overlapping targets between flaxseed bioactive compounds and constipation-related genes, with key hub targets including TP53, CASP3, TNF, and IL6. KEGG pathway enrichment suggested that the PI3K/AKT signaling pathway may serve as a central regulatory axis. Western blot further confirmed that p-PI3K and p-AKT protein levels in the colon were reduced in constipated mice, whereas FPM administration markedly restored their expression, indicating activation of the PI3K/AKT pathway. Overall, these findings demonstrate that FPM alleviates constipation by improving stool characteristics, enhancing intestinal motility, and maintaining mucosal integrity, potentially via modulation of the PI3K/AKT pathway. This study provides new insights into the gastrointestinal benefits of flaxseed-derived functional foods and supports their development as dietary supplements for intestinal health.

Gastric ulcer (GU) is among the most prevalent digestive disorders globally. This study investigates the protective effects of canolol, a natural phenolic compound derived from crude rapeseed oil, on ethanol-induced GU in rats. Our results demonstrated that canolol pretreatment notably reduced gastric mucosal damage, as evidenced by lower ulcer indices and improved histopathological scores. Ethanol exposure severely disrupted the gastric mucosal defense systems, characterized by reduced gastric wall mucus secretion, lower NP-SH levels, suppressed heat shock protein 70 expression, and decreased gastric mucosal blood flow; however, these effects were counteracted by canolol pretreatment. Canolol also alleviated ethanol-induced inflammation by reducing the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), enhancing the level of the anti-inflammatory cytokine (IL-10), and normalizing myeloperoxidase activity in the gastric mucosa. Additionally, canolol enhanced antioxidant defenses by increasing the activities of antioxidant enzymes (SOD, CAT, and GPx) and the GSH level, thereby mitigating ethanol-induced oxidative stress in the stomach. Moreover, canolol suppressed ethanol-induced apoptosis in the gastric mucosa, evidenced by a decrease in TUNEL-positive areas and downregulation of the expression of apoptotic markers BAX and caspase-3. Mechanistically, canolol substantially reduced the activities of p38 MAPK and NF-κB, consequently preventing NLRP3 activation. These findings indicate that canolol has potential benefits in preventing the onset and progression of ethanol-induced GU by inhibiting the p38 MAPK/NF-κB/NLRP3 pathway.

Inflammatory bowel disease (IBD) is often accompanied by secondary liver injury which further evolves into various hepatobiliary disorders. The pathogenesis of secondary liver injury involves many different mechanisms including inflammation, pyroptosis, oxidative stress, and heat shock response. Here, we tested the effect of administration of phenethyl isothiocyanate (PEITC) on secondary liver injury in DSS-induced IBD mice. PEITC supplementation reversed liver injury as determined by hepatic injury-related parameters and histopathological examinations. Severe hepatic inflammation with IBD, evidenced by ubiquitously distributed activated macrophages, increased secretion of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), enhanced expression of inflammation-related proteins (iNOS and COX-2), and augmented activation of the TLR4/NF-κB signaling pathway, was inhibited by PEITC treatment. PEITC also prevented IBD-induced increases in pyroptosis and oxidative stress in the liver. In addition, impairments of hepatic heat shock response elicited by IBD were restored by PEITC treatment. Taken together, these results suggested that PEITC may be effective as a therapeutic reagent to attenuate secondary liver injury caused by IBD.

Dietary supplementation with plant-derived α-linolenic acid (ALA), relying on its metabolic conversion into n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFAs), has the potential to optimize the dietary fatty acid profile and alleviate the global issue of insufficient n-3 LCPUFAs intake. Current research investigates the effects of flax lignans, with varying doses and structures, on the intestinal digestion-absorption and lymph-blood transport of ALA in sunflower phospholipid-stabilized nanoemulsions. The results indicated that the incorporation of flax lignans at various doses did not significantly alter the physical properties of nanoemulsions. However, medium and high doses of flax lignans, especially those partitioned within the aqueous phase and interface, reduced the release of free fatty acids and ALA content in micelles by potentially inhibiting enzyme activity during in vitro digestion. Meanwhile, intragastric administration of medium- or high-dose flax lignan-nanoemulsions decreased serum triglyceride, total cholesterol, and ALA levels, suggesting an inhibition of lymph-blood transport of ALA-containing chylomicrons. In contrast, the co-delivery of low-dose lignan-nanoemulsions increased serum ALA levels, particularly in flax lignan macromolecule (FLM, +31.4 %) and secoisolariciresinol (SECO, +39.6 %) nanoemulsions groups. Further results revealed that low-dose lignans enhanced ALA bioavailability (14.6 %-45.9 %), acting in a "rate-decelerating but efficiency-enhancing" manner based on the area under the blood concentration-time curve, accompanied by significant effects of FLM and SECO. Therefore, regulating the intestinal digestion and absorption of ALA-containing nanoemulsions may be an effective strategy to improve ALA lymph-blood transport and potential substrate levels for hepatic metabolic conversion. This research supports designing precise dietary delivery systems to improve ALA bioavailability.

Dietary supplementation with plant-derived α-linolenic acid (ALA) has the potential to alleviate the insufficient intake of global n-3 long-chain polyunsaturated fatty acids (n-3 LCPUFAs), but faces the bottleneck of high β-oxidation consumption, oxidative susceptibility, and low conversion efficiency. The current study investigated how flax lignans with different degrees of polymerization and glycosylation affect the conversion of ALA to n-3 LCPUFAs in mice over 35 days of administering sunflower phospholipid-stabilized flaxseed oil nanoemulsions. Results showed that flax lignan macromolecules (FLM) increased hepatic protein expression of elongase of very long chain fatty acid 5 (Elovl5, 24.2%) and fatty acid desaturase 2 (Fads2, 44.7%), thereby positively regulating ALA conversion pathways and raising serum eicosapentaenoic acid (EPA) levels (52.7%) via liver lipid re-efflux. Secoisolariciresinol diglucoside (SDG) enhanced ALA desaturation by upregulating hepatic protein expression of Fads1 (30.4%) and Fads2 (45.6%), increasing serum EPA levels (55.9%) and hepatic docosahexaenoic acid (DHA) levels (10%). Secoisolariciresinol (SECO) elevated hepatic protein expression of Elovl2 (30.7%), Elovl5 (11.7%), Fads1 (37.9%), and Fads2 (24.1%), but also increased carnitine palmitoyltransferase 1a (45.2%), leading to decreased ALA, EPA, and DHA levels in serum and liver. Therefore, in comparison, FLM and SDG emerge as the dominant structural units that positively regulate the conversion of ALA. These findings lay a groundwork for designing precise dietary delivery systems to enhance the conversion to n-3 LCPUFAs.

The brominated flame retardant 2,2′,4,4′-tetrabromodiphenyl ether (PBDE-47) is a ubiquitous environmental pollutant that causes neurotoxicity. However, incomplete understanding of the underlying mechanisms has hampered the development of effective intervention strategies. Oxidative stress and related cell death are the modes of action for PBDE-47 neurotoxicity, which are also the characteristics of ferroptosis. Nonetheless, the role of ferroptosis in PBDE-47-induced neurotoxicity remains unclear. In the present study, we found that PBDE-47 triggered ferroptosis in neuron-like PC12 cells, as evidenced by intracellular iron overload, lipid peroxidation, and mitochondrial damage. This was confirmed by ferroptosis inhibitors including the lipid reactive oxygen species scavenger ferrostatin-1 and iron chelator deferoxamine mesylate. Mechanistically, PBDE-47 impaired ferritinophagy by disrupting nuclear receptor coactivator 4-mediated lysosomal degradation of the iron storage protein ferritin. Moreover, PBDE-47 disturbed iron metabolism by increasing cellular iron import via upregulation of transferrin receptor 1 and decreasing cellular iron export via downregulation of ferroportin 1 (FPN1). Intriguingly, rescuing lysosomal function by overexpressing cathepsin B (CatB) mitigated PBDE-47-induced ferroptosis by partially restoring dysfunctional ferritinophagy and enhancing iron excretion via the upregulation of FPN1. However, FPN1 knockdown reversed the beneficial effects of CatB overexpression on the PBDE-47-induced iron overload. Finally, network pharmacology integrated with experimental validation revealed that Canolol, the main phenolic compound in canola oil, protected against PBDE-47-evoked iron overload, resulting in ferroptosis by restoring defective ferritinophagy and improving abnormal iron metabolism via lowering iron uptake and facilitating iron excretion. Overall, these data suggest that ferroptosis is a novel mechanism of PBDE-47-induced neuronal death and that manipulation of ferritinophagy and iron metabolism via Canolol represents a promising therapeutic strategy.

N-3 long-chain polyunsaturated fatty acids (n-3 LCPUFAs) are essential for physiological requirements and disease prevention throughout life but are not adequately consumed worldwide. Dietary supplementation with plant-derived α-linolenic acid (ALA) has the potential to rebalance the fatty acid profile and enhance health benefits but faces challenges such as high β-oxidation consumption, low hepatic conversion efficiency, and high oxidative susceptibility under stress. This review focuses on the metabolic fate and potential regulatory targets of ALA-containing lipids in vivo, specifically the pathway from the gastrointestinal tract to the lymph, blood circulation, and liver. We propose a hypothesis that positively regulates the conversion of ALA into n-3 LCPUFAs based on the model of "fast" or "slow" absorption, transport, and hepatic metabolic fate. Furthermore, the potential effects of dietary nutrients on the metabolic conversion of ALA into n-3 LCPUFAs are discussed. The conversion of ALA is differentially regulated by structured lipids, phospholipids, other lipids, carbohydrates, specific proteins, amino acids, polyphenols, vitamins, and minerals. Future research should focus on designing a steady-state and precise delivery system for ALA, coupled with specific nutrients or phytochemicals, to effectively improve its metabolic conversion and ultimately achieve synergistic regulation of nutrition and health effects.

Walnut oil (WO), known for abundant polyunsaturated fatty acids and an array of bioactive substances such as tocopherols, phytosterols, squalene, melatonin, and polyphenols, which is endowed with numerous health advantages. The primary objective of this research was to ascertain the impact of WO on cognitive deficits in learning and memory impairment mice caused by scopolamine (SCOP). The Morris water maze and the step-down avoidance test were utilized to assess the memory and learning capabilities. WO notably counteracted the detrimental effects of SCOP on learning and memory in the Morris water maze, as indicated by a reduction in escape latency and swimming distance. Likewise, WO administration led to a notably reduced number of errors in training trial and an increased latency in testing trial when compared to the SCOP group in the step-down avoidance test,. Moreover, WO activated the cholinergic system of the brain by upregulating choline acetyltransferase activity and reducing acetylcholinesterase activity. These results suggest that WO has the potential to protect against memory decline in mice, offering a promising strategy for the prevention of memory-related disorders.

IntroductionSaccharomyces boulardii (S. boulardii) has shown clinical beneficial effect in inflammatory bowel diseases recently. However, the underlying mechanisms remain incompletely understood. The aim of present study was to tested whether S. boulardii targets gut microbiota to protect against the development of experimental colitis in mice. MethodsFemale C57BL/6 mice were gavaged with S. boulardii for 3 weeks before being challenged with dextran sulphate sodium to induce ulcerative colitis. Bodyweight, diarrhea severity, intestinal permeability, colonic histopathology, colonic inflammatory status, and epithelial cell death of mice were examined. The fecal microbiota and its metabolomic profiles were detected by 16S rDNA sequencing and UPLC-MS, respectively. Results and DiscussionSupplementation with S. boulardii significantly prevented weight loss and colon shortening, lowered colonic inflammation, ameliorated epithelial injury, and enhanced the intestinal barrier integrity in colitis mice. By inhibiting the abundance of pathogenic bacteria and increasing the probiotics abundance, S. boulardii improved the microbial diversity and restored the microbiota dysbiosis. Moreover, it also modulated microbial metabolome and altered the relative contents of metabolites involving amino acids, lipids, energy and vitamin metabolisms. These yeast-driven shifts in gut flora and metabolites are were associated with each other and with the inflammation profile in colitis. Collectively, S. boulardii exerts protective effects on colitis in mice by reshaping gut microbiome and its metabolic profile, indicating it as a promising therapeutic avenue.

INTRODUCTION:Diminished brain insulin sensitivity is associated with reduced cognitive function. Docosahexaenoic acid (DHA) is known to maintain normal brain function. OBJECTIVES:This study aimed to determine whether DHA impacts hippocampal insulin sensitivity and cognitive function in aged rats fed a high-fat diet (HFD). METHODS:Eight-month-old female Sprague-Dawley rats were randomly divided into three groups (n = 50 each). Rats in the aged group, HFD group, and DHA treatment group received standard diet (10 kcal% fat), HFD (45 kcal% fat), and DHA-enriched HFD (45 kcal% fat, 1% DHA, W/W) for 10 months, respectively. Four-month-old female rats (n = 40) that received a standard diet served as young controls. Neuroinflammation, oxidative stress, amyloid formation, and tau phosphorylation in the hippocampus, as well as systemic glucose homeostasis and cognitive function, were tested. RESULTS:DHA treatment relieved a block in the insulin signaling pathway and consequently protected aged rats against HFD-induced hippocampal insulin resistance. The beneficial effects were explained by a DHA-induced decrease in systemic glucose homeostasis dysregulation, hippocampal neuroinflammation and oxidative stress. In addition, DHA treatment broke the reciprocal cycle of hippocampal insulin resistance, Aβ burden, and tau hyperphosphorylation. Importantly, treatment of model rats with DHA significantly increased their cognitive capacity, as evidenced by their increased hippocampal-dependent learning and memory, restored neuron morphology, enhanced cholinergic activity, and activated cyclic AMP-response element-binding protein. CONCLUSION:DHA improves cognitive function by enhancing hippocampal insulin sensitivity.

对褪黑素改善认知作用的研究进展进行综述,为褪黑素的进一步开发利用提供科学依据.

The International Symposium on Lipid Science and Health (ISLSH) has been organized annually by the Oil Crops Research Institute of Chinese Academy of Agricultural Sciences (OCRI-CAAS) since 2016. The purpose of the symposium was to bring together the leading lipid science and health researchers throughout the world to discuss the current state of knowledge as well as research needs with respect to chemistry and beneficial health properties of lipids. The Fifth International Symposium on Lipid Science and Health was held on October 2020 in Wuhan, Hubei, China. Speakers from China, the United States, Australia, Finland, and other countries delivered wonderful presentations. The presentations covered such diverse topics as lipid profiling and characterization, lipid preparation and modification, lipid improvement and regulation, and lipid nutrition and health. As a record of the symposium proceedings, this special issue comprises a selection of 27 papers from oral presentations and poster contributions and is prefaced by this introduction.

二十八烷醇主要通过调控机体能量代谢、抗氧化、减少代谢物积累和加强内环境稳定性等起到抗疲劳作用.对二十八烷醇抗疲劳作用机制的深入研究,对于进一步了解二十八烷醇的疲劳机制和推广应用具有重要意义.

Flax lignans (SDG) and sinapic acid (SA) both have the function of antioxidation and anti-inflammation. However, previous studies have focused mainly on biochemical measurements, gene expression analysis, and clinical assessments. There are limited studies that systematically reveal the underlying mechanism of the anti-inflammation effect of SDG or SA from the lipidomic point of view. Herein, the integrated lipidomic profiling platform was used for the analysis of free fatty acids (FFAs), phospholipids (PLs), triacylglycerols (TAGs), and oxylipins in high-fat (HF)-diet-fed mice after SDG or SA administration. Dietary supplementation of SDG or SA downregulated the levels of total TAGs and FFAs in the ApoE(-/-) mice model. Furthermore, 28 potential lipids were screened out and considered as key evaluation factors to understand the anti-inflammation function and mechanism of SDG and SA. The results indicated that the anti-inflammatory effect of SDG and SA was principally exerted via regulation of lipid homeostasis.

The International Symposium on Lipid Science and Health (ISLSH), which was organized annually by Oil Crops Research Institute of Chinese Academy of Agricultural Sciences (OCRI-CAAS) since 2016, has gained a strong reputation and attracted hundreds of delegates from around the world for discussion of lipid research trends and advances every year, to promote research and academic exchanges in the fields of lipid science and health. The 5th International Symposium on lipid Science and Health was successfully held in Wuhan, China, from October 23rd to 25th, 2020, to celebrate the 60th anniversary of OCRI-CAAS. The two-day symposium gathered well-known experts specialized in lipid science to share the current state of lipid research with emphasis on aspects covering: (1) lipid profiling and characterization, (2) lipid preparation and modification, (3) lipid improvement and regulation, and (4) lipid nutrition and health. The symposium was conducted by a combination of on-site and network meeting. More than 250 distinguished delegates from academia and industry participated in the on-site multidisciplinary meeting, and thousands of scholars attended the virtual event. This paper is as a record of the symposium proceedings and a brief summary of the advances and trends in 4 aspects of lipid science and health.