内容: In previous research, we demonstrated that long-term consumption of thermally oxidized oil leads to neuroinflammation and anxiety in mice. Therefore, in this study, we employed polar lipid components from thermo-induced oxidized oil to induce neurodamage. Behavioral assessments revealed that both the linoleic acid and AUDA (a classical inhibitor of soluble epoxide hydrolase) groups exhibited significantly reduced anxiety-like behaviors compared to the model group (P < 0.05). Immunofluorescence analysis indicated that microglial activation in the hippocampus was attenuated in both the linoleic acid and AUDA groups relative to the model group, accompanied by a reduction in the mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, NOS2, TNF-α) and an upregulation of neuroprotective factors (IL-4, IL-10, BDNF). Lipidomic profiling of hippocampal tissue revealed that the lipid composition of the linoleic acid group closely resembled that of the AUDA group, with a significant downregulation of cardiolipin (CL) compared to the control group, consistent with alterations in the membrane potential channel receptor TRPC1. Both linoleic acid and AUDA inhibited the mRNA expression of EPHX2, leading to an increase in epoxyeicosatrienoic acids (EETs) levels. Furthermore, linoleic acid upregulated the expression of cytochrome P450 enzymes (CYP2J6) and lipoxygenase (LOX2S), which further upregulated the synthesis of EETs, and increased the content of 9-HODE and 13-HODE. These findings collectively suggest that linoleic acid alleviates neuroinflammation by modulating microglial differentiation and attenuates neurodegeneration induced by thermally oxidized oil through the regulation of arachidonic acid metabolism and the linoleic acid metabolic pathway, leading to the production of neuroprotective lipid mediators. Therefore, linoleic acid may serve as a potential neuro-nutrient for the treatment of anxiety disorders. This provided a scientific basis for the development of specialized medical foods aimed at protecting neural health.

内容: High-fat diets (HFD) disrupt lipid homeostasis, posing major public health risks. This study investigated the effect of ACA-DK, an insoluble dietary fiber derived from Antrodia camphorata, on HFD-induced dyslipidemia. We demonstrate that ACA-DK effectively alleviates HFD-induced dyslipidemia in mice, counteracting metabolic disorders, aberrant blood lipids, and weight gain. Mechanistically, ACA-DK modulates triglycerides, phosphatidylcholine, and phosphatidylethanolamine via glycerophospholipid/choline/linoleic acid metabolism pathways, while rectifying gut dysbiosis through selective reduction of pro-inflammatory genera (Oscillibacter, Ruminiclostridium, Negativibacillus, Ruminococcaceae and Helicobacter). Integrated analysis identifies Ruminococcaceae and Helicobacter as key mediators of ACA-DK’s lipid-regulatory effects, establishing microbiota-directed therapy as a strategy against dyslipidemia. We thus propose ACA-DK as a microbiota-directed dual-target therapy, simultaneously reprogramming host lipid metabolism and gut ecology to combat diet-induced metabolic diseases. These findings suggest that ACA-DK is a promising prebiotic dietary fiber for ameliorating HFD-induced lipid metabolic disorders, with potential for future development into functional foods or supplements.

内容: To obtain protease- and lipase-producing halotolerant/halophilic strains suitable for shrimp paste (SP) fermentation, the microbial community structure and enzyme-producing microbial species were analyzed and predicted using metagenomics in 3 high-salt samples. Based on the linear salt gradient method, 128 strains were screened. Eight halotolerant/halophilic strains highly producing 2 types of enzymes were identified and inoculated into low-salt SP to assess the heterogeneity of SP. Physicochemical properties of SP indicated that Bacillus subtilis XJ-11, Virgibacillus halodenitrificans XJ-229, Piscibacillus halophilus XY-193, and Bacillus vallismortis HT-73 were more suitable for rapid fermentation of SP. Nutritional analysis showed that SP inoculated with V. halodenitrificans XJ-229 had the highest free amino acid content and SP inoculated with P. halophilus XY-193 had the highest unsaturated fatty acid content. The former had prominent umami, sweetness, and meaty aroma, weak bitterness and fishy flavor, and the closest flavor to the control (CP) based on sensory evaluation and E-nose analysis. A total of 61 volatile compounds were detected in all samples by SPME-GC-MS, of which 32, 23, 40, 24, and 28 were detected in the CP and SP inoculated with B. subtilis XJ-11, V. halodenitrificans XJ-229, P. halophilus XY-193, and B. vallismortis HT-73, respectively, with 12, 11, 12, 9, and 9 key flavor compounds. Among several samples, the highest levels of pyrazines, aldehydes, alcohols, and ketones were found in SP inoculated with B. subtilis XJ-11, V. halodenitrificans XJ-229, P. halophilus XY-193, and B. vallismortis HT-73, respectively. These results suggested that inoculation of different enzyme-producing halotolerant/halophilic strains resulted in differences in SP quality and main flavors. This study provides some references for process control and interpretation of heterogeneous mechanisms in low-salt SP fermented by inoculated strains.

内容: Artemisia argyi (A. argyi) is a Chinese herbal medicine with reported anti-inflammatory effects. In this study, the A. argyi was extracted with water and ethanol, and the concentrations of 35 flavonoids in A. argyi water extract (WE) and ethanol extract (EE) were measured via targeted metabolomics. The antioxidant and anti-inflammatory activities of both WE and EE were firstly explored in vitro via chemical assays and cellular experiment, respectively. Both WE and EE showed significant 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), ·OH, and O2· radical scavenging ability in a dose-dependent manner, and reduced the levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-22 (IL-22) in lipopolysaccharide (LPS) induced RAW264.7 cell model. In addition, the in vivo anti-colitis activity of both extracts was investigated in dextran sulfate sodium (DSS)-induced colitis mice, and the underlying mechanisms were elucidated by 16S rDNA sequencing and targeted metabolomics. We found that both WE and EE relieved colitis in mice, characterized by decreased disease activity index, increased colon length, improved pathological changes in colon tissue, while EE showed better anti-colitis activity. In addition, both 16S rDNA sequencing and targeted bile acids metabolomics indicated EE modulated gut microbiota and specifically increased the abundance of lithocholic acid (LCA), which might contribute to intestinal barrier function improvement via up-regulating the expression of colonic farnesoid X receptor (FXR). In summary, this study identified the anti-colitis mechanism of A. argyi EE by modulating gut microbiota, facilitating the production of LCA, activating FXR and improving intestinal barrier function.

内容: Alzheimer’s disease (AD) is a serious disease associated with cognitive impairment, and synaptic loss and amyloid-beta (Aβ) deposition are closely related to its pathogenesis. Docosahexaenoic acid (DHA) has been reported to alter the cognitive impairment associated with aging and reduce the risk of long-term development of AD. However, the effects of Aβ on synapses and whether DHA has a protective effect on synapses remain unclear. In this study, APPSwe/PSEN1dE9 transgenic and wild type mice were used as experimental subjects to explore the effect of DHA on synaptic structure and function damaged by Aβ. Results showed that a large amount of Aβ was deposited in the brain of AD mice, and DHA intervention decreased the Aβ deposition (P < 0.05). DHA decreased the apoptosis of nerve cells and the oxidative stress level induced by Aβ (P < 0.01). Transmission electron microscopy results showed that DHA improved the synaptic structure and number, and the expression of synaptophysin was significantly upregulated by DHA (P < 0.01). Besides, neurotransmitter release was regulated after DHA intervention, including the decreased Glu level and increased γ-aminobutyric acid level, as well as the activity of ATPase was also increased by DHA. Importantly, the phosphorylation levels of tyrosine kinase B (TrkB), phospholipase C-gamma-1, calcium/calmodulin-dependent protein kinase Ⅱ, extracellular regulated protein kinases (ERK1/2), and cAMP-response element binding protein (CREB) were upregulated by DHA (P < 0.01). These data indicated that DHA could improve synaptic structure and function through the TrkB-Erk1/2-CREB pathway, thus playing a positive role in the pathological process of AD.