Guiling Li

Previous transcriptomic analysis revealed that eicosapentaenoic acid (EPA) alters miRNA expression in HepG2 cells. Two key miRNA‐mRNA axes mediating EPA's antioxidant effects were identified. EPA was found to downregulate let‐7c‐3p, which directly targets mitochondrial transcription factor A (TFAM). Inhibiting let‐7c‐3p or overexpressing TFAM enhanced antioxidant capacity, reduced reactive oxygen species, improved mitochondrial function, and promoted mitochondrial biogenesis. In parallel, EPA was found to upregulate miR‐34c‐5p, which directly targets NAD‐Dependent Protein Deacetylase Sirtuin (SIRT1). This repression of SIRT1 is associated with increased activities of antioxidant enzymes, including catalase, superoxide dismutase, and glutathione peroxidase. These findings indicate a dual‐miRNA mechanism through which EPA alleviates oxidative stress via coordinated enhancement of mitochondrial biogenesis and enzymatic defenses.

Milk-derived extracellular vesicles (mEVs) are increasingly recognized as bioactive nanocarriers in dairy foods, but how industrial thermal processing reshapes their quality remains unclear. Here, we established a nano-flow cytometry (nFCM)-based single-particle strategy to evaluate mEVs from raw bovine milk and milk subjected to low-temperature long-time pasteurization, high-temperature short-time pasteurization, or ultra-high-temperature treatment. Thermal processing had limited effects on vesicle morphology and size distribution, yet it compromised several process-sensitive attributes, including surface protein presentation, miR-148a-positive subpopulations, gastrointestinal tolerance, epithelial uptake/transport, anti-inflammatory and antioxidant bioactivity. Multi-attribute profiling and multivariate analysis further distinguished treatment-specific quality signatures and revealed a cascade-like decline from vesicle preservation to cellular bioactivity. This platform identifies process-sensitive quality attributes of mEVs and provides a single-particle analysis strategy for linking food processing to the structural, molecular, and functional properties of food-derived extracellular vesicles, supporting processing optimization, bioproduct development, and quality control.

Curcumin, the major bioactive polyphenol derived from the edible rhizome turmeric (Curcuma longa L.), is recognized for its health-promoting properties. Despite well-documented antioxidant effects, its molecular mechanisms, particularly those involving post-transcriptional regulation, remain incompletely understood. This in vitro study identifies a novel microRNA-mediated pathway contributing to the antioxidant activity of curcumin in human hepatic LO2 cells. Curcumin treatment downregulated the stress-responsive microRNA miR-22-3p. Bioinformatics analysis and a dual-luciferase reporter assay identified malonyl-CoA-acyl carrier protein transacylase (MCAT), a mitochondrial enzyme, as a direct target of miR-22-3p. Modulation of this axis reduced intracellular reactive oxygen species (ROS), enhanced total reducing capacity, increased activities of key antioxidant enzymes (SOD, CAT, GPx), and improved mitochondrial bioenergetics without altering membrane potential. Crucially, siRNA-mediated knockdown of MCAT attenuated the ROS-scavenging effect of curcumin. These findings reveal a mechanistic pathway wherein curcumin downregulates miR-22-3p, resulting in upregulation of MCAT and enhanced mitochondrial antioxidant defense. This work broadens the understanding of curcumin’s bioactivity from direct radical scavenging to include the post-transcriptional fine-tuning of mitochondrial metabolism. The study establishes a molecular framework for further exploration of curcumin’s potential in alleviating oxidative stress.

Background: Ulcerative colitis is a chronic inflammatory disease affecting the colon and is supposed to be related to intestinal barrier dysfunction and gut microbiota disorders. Previous study identified the potential antioxidant effects of the peptide GFGFGGF derived from Quasipaa spinosa skin (QSP), but its other bioactive functions require further research. The aim of this study was to assess the function of QSP in a mouse model of colitis induced by dextran sodium sulfate (DSS). Results: The results showed that QSP ameliorated the symptoms of DSS‐induced colitis in mice, such as weight loss, colon shortening, splenomegaly and histopathological changes. Further investigations revealed that QSP treatment suppressed the production of pro‐inflammatory cytokines (IL‐1 β , IL‐6 and TNF‐ α ). Results from RT‐qPCR and Western blot analyses demonstrated that QSP inhibited the activation of the NF‐ κ B signaling pathway and reduced the mRNA levels of its downstream inflammation‐related genes (IL‐1 β , IL‐6 and TNF‐ α ). Meanwhile, QSP increased the mRNA level of tight junction proteins (ZO‐1, Occludin) and adherens junction proteins (E‐cadherin) to maintain the integrity of the colonic barrier thus improving intestinal health. Meanwhile, QSP treatment modulated the composition of the intestinal microbiota, reversing the relative abundance of harmful and beneficial bacteria, and increased the levels of short‐chain fatty acids. Conclusion: Our results indicated that peptide GFGFGGF had a notable function in preventing colitis induced by DSS. The restoration of the gut barrier and the regulation of gut microbiota were achieved by it, and it may be a promising prebiotic for the treatment of colitis. © 2025 Society of Chemical Industry.

Given the worldwide epidemic of overweight and obesity among children, evidence-based dietary recommendations are fundamentally important for obesity prevention. Although the significance of the human gut microbiome in shaping the physiological effects of diet and obesity has been widely recognized, nutritional therapeutics for the mitigation of pediatric obesity globally are only just starting to leverage advancements in the nutritional microbiology field. In this review, we extracted data from PubMed, EMBASE, Scopus, Web of Science, Google Scholar, CNKI, Cochrane Library and Wiley online library that focuses on the characterization of gut microbiota (including bacteria, fungi, viruses, and archaea) in children with obesity. We further review host-microbe interactions as mechanisms mediating the physiological effects of dietary fibers and how fibers alter the gut microbiota in children with obesity. Contemporary nutritional recommendations for the prevention of pediatric obesity are also discussed from a gut microbiological perspective. Finally, we propose an experimental framework for integrating gut microbiota into nutritional interventions for children with obesity and provide recommendations for the design of future studies on precision nutrition for pediatric obesity.

The escalating prevalence of obesity poses significant health challenges due to its direct association with various diseases. Most existing medications, such as appetite suppressants and fat absorption inhibitors, suffer from limited effectiveness and undesirable side effects. Here, inspired by the versatile metabolic effects of turmeric, we developed a naturally derived nanoformulation of "Reconstructed Turmeric-derived Nanovesicles (Rec-tNVs)" for obesity treatment. Employing quantitative nanoflow cytometry, a four-orders-of-magnitude increase in curcumin content (∼10⁸ molecules per particle) was identified in individual Rec-tNVs compared to their ultracentrifugation-isolated counterparts. Rec-tNVs, featuring highly aggregated curcumin arrangements and other coencapsulated bioactive compounds, demonstrated a dose-dependent lipid-lowering effect in mature 3T3-L1 cells by promoting lipolysis, suppressing lipogenesis, inducing adipocyte browning, and triggering apoptosis after internalization via multiple pathways. In vivo experiments revealed that Rec-tNVs alleviated obesity more effectively than free curcumin and achieved weight reductions of 18.68 and 14.56% through intragastric and subcutaneous delivery, respectively, in high-fat-diet mouse models over a four-week treatment period. These effects were attributed to targeted actions on adipose tissues and systemic impacts on metabolism and gut microbiota composition. Overall, this study underscores the multifaceted antiobesity efficacy of Rec-tNVs, and offers a promising paradigm for developing plant-derived nanovesicle-based therapeutics.

Melanosomes are specialized membrane-bound organelles where melanin is synthesized and stored. The levels of melanin can be effectively reduced by inhibiting melanin synthesis or promoting melanosome degradation via autophagy. Ceramide, a key component in the metabolism of sphingolipids, is crucial for preserving the skin barrier, keeping it hydrated, and warding off the signs of aging. Our preliminary study indicated that a long-chain C22-ceramide compound (Ehux-C22) isolated from the marine microalga Emiliania huxleyi, reduced melanin levels via melanosomal autophagy in B16 cells. Recently, microRNAs (miRNAs) were shown to act as melanogenesis-regulating molecules in melanocytes. However, whether the ceramide Ehux-C22 can induce melanosome autophagy at the post-transcriptional level, and which potential autophagy-dependent mechanisms are involved, remains unknown. Here, miR-199a-3p was screened and identified as a novel upregulated miRNA in Ehux-C22-treated B16 cells. An in vitro high melanin expression model in cultured mouse melanoma cells (B16 cells) was established by using 0.2 μM alpha-melanocyte-stimulating hormone(α-MSH) and used for subsequent analyses. miR-199a-3p overexpression significantly enhanced melanin degradation, as indicated by a reduction in the melanin level and an increase in melanosome autophagy. Further investigation demonstrated that in B16 cells, Ehux-C22 activated miR-199a-3p and inhibited mammalian target of rapamycin(mTOR) level, thus activating the mTOR-ULK1 signaling pathway by promoting the expression of unc-51-like autophagy activating kinase 1 (ULK1), B-cell lymphoma-2 (Bcl-2), Beclin-1, autophagy-related gene 5 (ATG5), and microtubule-associated protein light chain 3 (LC3-II) and degrading p62. Therefore, the roles of Ehux-C22-regulated miR-199a-3p and the mTOR pathway in melanosomal autophagy were elucidated. This research may provide novel perspectives on the post-translational regulation of melanin metabolism, which involves the coordinated control of melanosomes.

A silyl radical-induced cascade silylation/cyclization of 1,7-dienes to construct valuable Si-containing benzo[b]azepin-2-ones is presented.