Aging is one of the causes of cognitive dysfunction, which seriously affects people's quality of life. Unsaponifiable matter (USM) has antioxidant potential, but the molecular mechanisms that ameliorate aging and cognitive dysfunction are unknown. In this study, we used a galactose-induced brain aging mouse model and systematically analyzed the mechanism of USM in delaying aging in mice by detecting changes in serum and brain by metabolomics and transcriptomics. USM was compared with the model group, and non-targeted metabolomics identified 68 (15 up-regulated, 53 down-regulated) differentially metabolites, and transcriptomics identified 303 differentially expressed genes (228 up-regulated, 75 down-regulated). Combined multi-omics analyses showed that USM maintains normal brain function by regulating glycolytic processes, the tricarboxylic acid cycle (TCA), tryptophan metabolism, pyrimidine metabolism, the alanine, aspartate, and glutamate metabolism, and p38 mitogen-activated protein kinase (p38 MAPK) pathway. Meanwhile, USM increased neurotransmitter release from GABAergic synapses and cholinergic synapses by regulating synaptic vesicle cycling. In summary, USM increased energy metabolism and enhanced brain nerve signaling in the mouse brain, thereby delaying brain aging. This investigation offers novel perspectives into the molecular mechanism of USM to mitigate brain aging.

Obesity, driven by unhealthy dietary patterns, has become a global health threat. Mushroom polysaccharides (MPs) exhibits promising protective effects against obesity. This review elucidate the potential anti-obesity mechanisms of MPs, focusing on their ability to modulate lipid metabolism, cholesterol homeostasis, gut microbiota, mitochondrial function, and oxidative stress. Specifically, MPs can protect against diet-induced obesity by improving lipid and cholesterol metabolism. Additionally, MPs improve obesity by modulating gut microbiota composition, which plays a pivotal role in lipid and energy metabolism. Moreover, diet-induced mitochondrial dysfunction, endoplasmic reticulum stress, and oxidative stress disrupt metabolic homeostasis through direct lipid dysregulation and inflammation-mediated pathways. MPs mitigate these effects by enhancing mitochondrial function, alleviating ER stress, and reducing oxidative stress, thereby restoring metabolic balance. This review presents a comprehensive discussion on MPs research as functional compounds utilized in food and medicine and could be beneficial for obesity and related metabolic disorders.

Penicillium expansum, a common spoilage organism in postharvest fruits, can cause fruit decay and deterioration and endanger human health. It is of great significance to investigate the antimicrobial mechanism of the antimicrobial peptide from Paenibacillus ehimensis on P. expansum spores. The antimicrobial activity of the antimicrobial peptide against P. expansum spores was determined by using the two-fold dilution method as well as measuring the time-killing curve. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to evaluate the effect of the antimicrobial peptide on the ultrastructure of P. expansum spores. The effects of the antimicrobial peptide on the cell membrane and reactive oxygen species (ROS) accumulation of P. expansum were analyzed by fluorescence probes. The results showed that the minimum inhibitory concentration (MIC) of the antimicrobial peptide against P. expansum spores was 3.5 AU/mL. The spore germination rate was significantly decreased by 28.30%, 84.57% and 100% by the antimicrobial peptide at concentrations of 0.5 MIC, 1 MIC and 2 MIC compared with the blank control (P < 0.05). After treatment with the antimicrobial peptide, the spores appeared seriously sunken, the intracellular contents were leaked out, and the morphology and structure were changed. The antimicrobial peptide damaged the cell wall of P. expansum, resulting in the leakage of alkaline phosphatase. The antimicrobial peptide depolarized the cell membrane potential in a dose-dependent manner, and increased the cell membrane permeability, leading to K⁺ leakage. The fluidity of the cell membrane was increased, which in turn resulted in a significant decrease in DPH fluorescence intensity (P < 0.05). The integrity of the cell membrane was damaged by the antimicrobial peptide, so the fluorescence intensity of SYTOX-Green and the contamination rate of PI were increased. Moreover, the antimicrobial peptide at 1 MIC and 2 MIC increased the fluorescence intensity of DCFH-DA significantly (P < 0.05) and resulted in ROS accumulation, which affected the physiology and metabolism of P. expansum spores. This study indicated that the target sites of the antimicrobial peptide against P. expansum spores were mainly the cell membrane and ROS metabolism.

This study investigated the inhibitory effect of antimicrobial peptide from Paenibacillus ehimensis on the biofilms of Candida albicans by the microdilution and time-kill curve assays. Microscopic observation was conducted to assess the impact of the peptide on the formation of C. albicans germ tube and hyphae. Additionally, the 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) assay was employed to investigate the influence on the formation of C. albicans biofilms, pre-formed biofilms, and the clearance rate of mature biofilms. Fluorescent probes were utilized to observe the alteration in the structure of biofilms and the status of intracellular fungal entities. The number of viable cells in biofilms was measured by the spread plate method, and real-time polymerase chain reaction (PCR) was employed to determine the expression levels of genes associated with biofilm formation. The results showed that the minimum inhibitory concentration of the antimicrobial peptide against C. albicans was 8.28 AU/mL. This peptide reduced the rate of germ tube formation in C. albicans, and prevented the formation of hyphae, making it exist in the form of yeasts. Furthermore, the antimicrobial peptide influenced both the formation and eradication of biofilms and disrupted the structural integrity of biofilms after a short duration, leading to damage and even death of C. albicans, and reducing cell counts in biofilms. The antimicrobial peptide reduced the expression levels of multiple genes related to biofilm formation (such as ALS1, ALS3, HWP1, EFG1, ECE1 and UME6), therefore inhibiting biofilm formation. The above findings demonstrated that antimicrobial peptide effectively inhibited the biofilm formation, mature biofilm clearance and the expression of biofilm-forming genes in C. albicans. This study lays a theoretical foundation for the development of novel antimicrobial agents against C. albicans and provides a basis for the prevention and control of foodborne pathogen contamination to ensure food quality and safety.

The neuroprotective effects of walnut protein hydrolysates (WPH) have been widely reported, and its antidepressant potential is worthing to exploring. In this study, a series of WPH were prepared by several group of complex hydrolysis and screened for potential antidepressant activity. The results showed that the hydrolyzed product (G2) from alkaline protease and pepsin had the most antidepressant potential. This is because G2 has anti-inflammatory effects and has a strong inhibitory effect on indoleamine 2,3-dioxygenase 1 (IDO1) activity at the chemical and cellular level, with a chemical IC₅₀ at 70.26 μg/mL and a cellular IC₅₀ at 65.29 μg/mL. G2 significantly improved chronic unpredictable mild stress (CUMS)-induced depressive behavior in mice. Trp targeted metabolomics analysis revealed that G2 reversed the CUMS-induced conversion of excess Trp to kynurenine (Kyn) and alleviated the Trp metabolic imbalance by inhibiting IDO1 activity. These findings suggest G2 alleviates depressive symptoms by inhibiting IDO1 and optimizing Trp metabolism, indicating its potential as a natural antidepressant functional food.

Aging is an inevitable biological phenomenon that involves a multitude of physiological alterations. Dietary interventions are being considered as potential strategies for delaying age-related dysfunction. Unsaponifiable matter (USM), a composition of highly active ingredients found in walnut oil, has demonstrated antioxidant effects. This study aims to explore the neuroprotective effects of USM on D-galactose-treated C57BL/6 mice and elucidate its underlying mechanism, which was validated in PC12 cells treated with D-galactose. The results of behavioral tests demonstrated that USM significantly improved cognitive deficits associated with aging. The morphological analysis demonstrated that USM effectively alleviated hippocampal neuronal damage, synaptic impairment, and mitochondrial dysfunction induced by D-galactose. Furthermore, USM significantly increases the antioxidant enzymes activity while reducing the malondialdehyde and reactive oxygen species levels. The results suggest that USM can mitigate age-related symptoms caused by D-galactose by activating the nuclear factor erythroid-2-related factor 2 signaling pathway, which enhances the expression of antioxidant enzymes, restore redox balance, and improves synaptic and mitochondrial functions. This has a positive on improving cognition and memory disorders in elderly mice.

Listeria monocytogenes is a worrisome food-borne pathogen threatening global food safety. Our previous study proved that lipopeptide brevilaterin B showed efficient antibacterial activity against L. monocytogenes by interacting with the cell membrane. This research further explored the antibacterial mechanism of brevilaterin B against L. monocytogenes at the sub-minimum inhibition concentration via transcriptomic analysis. Brevilaterin B induced growth inhibition rather than direct membrane lysis in L. monocytogenes at the minimum inhibitory concentration. Transcriptomic analysis showed 1779 difference expressed genes, including 895 up-regulated and 884 down-regulated genes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis indicated that brevilaterin B influenced multiple pathways of L. monocytogenes, including peptidoglycan biosynthesis, membrane transport (ATP-binding cassette transports, ion transport), cellular metabolism (amino acid and lipid metabolism), ATP synthesis, and activation of the stress response (quorum sensing and bacterial chemotaxis). In conclusion, brevilaterin B affects gene expression related to biosynthesis, transport and stress response pathways on the membrane of L. monocytogenes. The present work provides the first transcriptomic assessment of the antibacterial mechanism of lipopeptide brevilaterin B at the gene level.