锦州医科大学

A gold-doped MOF-79 composite was synthesized and subsequently applied as an electrochemical sensing material for the determination of quercetin in seawater. Considering that quercetin is widely used as a pharmaceutical compound and may pose potential ecological risks when released into aquatic environments, the development of a simple and reliable detection method was of practical significance. To this end, a novel Au@MOF-79 composite was prepared via a hydrothermal route and was characterized by scanning electron microscopy, high-resolution transmission electron microscopy, X-ray diffraction, and X-ray photoelectron spectroscopy. The obtained Au@MOF-79 was drop-cast onto a glassy carbon electrode to fabricate the Au@MOF-79/GCE sensor. Electrochemical measurements demonstrated that the Au@MOF-79/GCE exhibited enhanced electrocatalytic activity toward quercetin oxidation and enabled its quantitative determination using differential pulse voltammetry. A good linear relationship between the oxidation peak current and quercetin concentration was obtained in the range of 3.04 × 10⁻⁵ to 1.196 × 10⁻³ M, with a detection limit of 6.0 × 10⁻⁶ M. Furthermore, the sensor showed good repeatability and short-term operational stability, and maintained satisfactory analytical performance in seawater samples. The improved sensing performance was attributed to the synergistic effect between the porous MOF-79 framework and uniformly dispersed Au nanoparticles, which facilitated analyte enrichment and electron transfer. These results indicated that the Au@MOF-79-modified electrode had potential for the electrochemical detection of quercetin in complex aqueous environments.

OBJECTIVE:This study explores the molecular mechanism of HDAC5 in ferroptosis of intestinal epithelial cells in sepsis-induced acute intestinal injury. METHODS:A mouse model was established by cecal ligation and perforation (CLP) and an in vitro model of intestinal epithelial cells was induced by lipopolysaccharide (LPS). Immunohistochemistry, RT-qPCR, or Western blot determined the expressions of HDAC5, KLF4, and LncRNA MEG3 in cells. HDAC5 expression was reduced via lentivirus injection and siRNA transfection, followed by evaluation of intestinal tissue injury and cell injury, detection of Fe2+, ROS, GSH, and MDA levels, as well as detection of ACSL4 and SLC7A11 protein expressions. The permeability was evaluated by detecting the flux of fluorescein isothiocyanate-dextran. ChIP analyzed the enrichment of HDAC5 and H3K27ac on KLF4 promoter. The binding of KLF4 to LncRNA MEG3 promoter was verified by ChIP and dual luciferase assays. RIP and RNA pull down analyzed the binding of LncRNA MEG3 to LSD1. The enrichment of LSD1, H3K4me2, or H3K9me2 on ACSL4 or SLC7A11 promoter was analyzed by ChIP. RESULTS:HDAC5 expression was increased in intestinal tissues of CLP mice and LPS-induced cells, while KLF4 and LncRNA MEG3 expressions were decreased. Low expression of HDAC5 alleviated intestinal tissue injury, enhanced LPS-induced cell viability, and reduced ferroptosis. Mechanistically, HDAC5 inhibited KLF4 expression through deacetylation of H3K27ac, thereby suppressing transcriptional promotion of LncRNA MEG3 by KLF4, reducing recruitment of LSD1, enhancing H3K4me2 on ACSL4 promoter and H3K9me2 enrichment on SLC7A11 promoter, promoting ACSL4 and inhibiting SLC7A11 expression. CONCLUSION:HDAC5 promotes intestinal epithelial cell ferroptosis and exacerbates sepsis-induced acute intestinal injury by inhibiting KLF4/LncRNA MEG3 axis through deacetylation of H3K27ac.

Atherosclerosis (AS) is a chronic inflammatory disease driven by macrophages. While the RANK/RANKL signaling axis and SPP1 (osteopontin) are individually known to contribute to vascular inflammation, whether they function within a coordinated regulatory hierarchy in plaque macrophages remains unknown. This study investigates whether RANK defines a pro-inflammatory macrophage subset and whether SPP1 acts as a critical downstream effector within the RANK signaling pathway to promote AS progression. Plaque tissue samples were obtained from databases of atherosclerotic patients, experimental atherosclerotic animal models, and in vitro cell experiments to analyze the role of the RANK molecule and macrophages in atherosclerosis and to investigate its association with disease severity. Single-cell RNA sequencing, histological analysis, co-culture of ox-LDL with macrophages, and gene knockout animal experiments were employed to study the mechanism of RANK high expression on macrophages in atherosclerosis progression. We found that high expression of RANK is closely correlated with the severity of atherosclerosis. Single-cell transcriptomic analysis revealed that RANK⁺ cells are primarily enriched in macrophages, and RANK⁺ macrophages exhibit active metabolic and immune response pathways in AS. Cell communication analysis showed that RANK⁺ macrophages are closely associated with SPP1, with SPP1 being a key gene in RANK⁺ macrophages. Furthermore, the number of RANK⁺/SPP1⁺ macrophages increases with AS progression. Mechanistically, SPP1 is a downstream gene of RANK. RANK promotes AS progression by upregulating SPP1, acting through macrophage immunomodulatory pathways. Knocking out RANK in macrophages suppressed SPP1 expression and inhibited the ability of macrophages to phagocytose ox-LDL. Additionally, inhibiting RANK in mouse and rat AS models similarly suppressed SPP1 expression and reduced plaque formation, thereby delaying AS progression. This study establishes a previously unrecognized RANK–SPP1 signaling axis that functions as a macrophage-autonomous inflammatory amplifier in atherosclerosis. We demonstrate that RANK defines a distinct pro-inflammatory macrophage subset characterized by high metabolic and inflammatory pathway activity. Mechanistically, RANK transcriptionally upregulates SPP1 via the NF-κB pathway, and the accumulation of RANK⁺SPP1⁺ macrophages correlates with disease severity. Pharmacological inhibition of RANK signaling attenuates plaque progression in preclinical models, highlighting this axis as a potential therapeutic target for AS.

Carotid plaque instability is a critical precursor to ischemic stroke, but the role of trace elements in this process remains incompletely understood. This study aimed to evaluate the association between essential trace element mixtures (iron, copper, zinc, and selenium) and carotid plaque instability, with particular attention to metabolic context-dependent effects. Methods: We conducted a cross-sectional study of 1000 patients (56.8 ± 8.8 years) with carotid atherosclerotic plaques from Huludao Central Hospital. Participants were stratified into stable n = 536 and unstable(n = 464)groups based on carotid ultrasound assessment. Serum Fe, Cu, Zn, and Se were measured using inductively coupled plasma mass spectrometry. weighted quantile sum regression and restricted cubic spline evaluated element mixtures and dose-response relationships, stratified by smoking, hypertension, and diabetes.Results: Iron and copper exhibited significant positive linear associations with plaque instability (Q4 vs. Q1: OR = 5.39, 95

Metal-based nanomedicine, which involves nanoparticles (NPs) composed of metals such as gold, silver, iron, and platinum, has emerged as a promising approach in drug delivery, cancer therapy, imaging, and diagnostics. This review systematically examines a variety of metal-containing NPs (MNPs), including elemental metal NPs, metal oxides, metal-organic frameworks, nanozymes, and up-conversion NPs, highlighting their unique physicochemical properties and biomedical applications. The biological functions of MNPs, particularly in drug delivery, imaging, and therapeutic contexts, are critically discussed. Key engineering strategies aimed at optimizing targeted delivery, drug loading, responsive release, and biocompatibility are explored, with a focus on enhancing clinical outcomes. Recent advances underscore the potential of MNPs in innovative applications such as liquid biopsy, tumor imaging, chemotherapy, immunotherapy, physical therapy, and nanozyme-mediated treatments. Despite promising developments, clinical translation remains hindered by challenges such as toxicity, scalability, and regulatory hurdles. This review concludes with an outlook on future directions for MNPs, emphasizing their potential to revolutionize disease diagnosis and treatment through innovative biomaterial design and engineering. (c) 2026 Published by Elsevier B.V. on behalf of Chinese Chemical Society and Institute of Materia Medica, Chinese Academy of Medical Sciences.