FOOD CHEMISTRY
·
2025
·
IF 9.8
Zhe Sun,Yuanyuan Hui,Ding Yang,Lusha Wei,Ke Ren,Qianyi Mi,Bingqian Liu,Yiran Tian,Bini Wang
Aflatoxin M 1 (AFM 1 ) contamination in milk and dairy products poses a serious food safety concern, especially in regions with limited regulatory oversight. This study developed a zinc oxide–zirconium metal–organic framework (ZnO@PCN-777) for efficient AFM 1 removal from goat milk. The composite exhibited a high adsorption capacity of 112.87 mg g −1 . Kinetic modeling indicated that the adsorption followed a pseudo-second-order model, while isotherm analysis conformed to the Freundlich model, suggesting multilayer adsorption on a heterogeneous surface. X-ray photoelectron spectroscopy (XPS) analysis identified hydrogen bonding, π–π stacking interactions, and pore-filling effects as the primary mechanisms of AFM 1 adsorption, with their synergistic action enhancing overall efficiency. ZnO@PCN-777 maintained excellent reusability across 15 adsorption–desorption cycles. In real milk samples, adding 0.075 % ( w /w) of the adsorbent achieved a 93 % AFM 1 removal rate without affecting milk quality, demonstrating a strong potential for dairy detoxification applications.
研究领域:
食品科学与技术
·
环境化学
·
材料科学
·
毒理学
·
乳品安全
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产品关联
DOI
PubMed
高影响因子
Materials
·
2022
·Vol. 16
·期 1
·208
·
IF 3.748
Meinan Wan,Mo Xiong,Shouqin Tian,Xingzhu Chen,Bin Li,Xuesong Lu,Xiujian Zhao
VO2, as a promising material for smart windows, has attracted much attention, and researchers have been continuously striving to optimize the performance of VO2-based materials. Herein, nitrogen-incorporated VO2(M1) thin films, using a polyvinylpyrrolidone (PVP)-assisted sol–gel method followed by heat treatment in NH3atmosphere, were synthesized, which exhibited a good solar modulation efficiency (ΔTsol) of 4.99% and modulation efficiency of 37.6% at 2000 nm (ΔT2000 nm), while their visible integrated transmittance (Tlum) ranged from 52.19% to 56.79% after the phase transition. The crystallization, microstructure, and thickness of the film could be regulated by varying PVP concentrations. XPS results showed that, in addition to the NH3atmosphere-N doped into VO2lattice, the pyrrolidone-N introduced N-containing groups with N–N, N–O, or N–H bonds into the vicinity of the surface or void of the film in the form of molecular adsorption or atom (N, O, and H) filling. According to the Tauc plot, the estimated bandgap of N-incorporated VO2thin films related to metal-to-insulator transition (Eg1) was 0.16–0.26 eV, while that associated with the visible transparency (Eg2) was 1.31–1.45 eV. The calculatedEg1andEg2from the first-principles theory were 0.1–0.5 eV and 1.4–1.6 eV, respectively. The Tauc plot estimation and theoretical calculations suggested that the combined effect of N-doping and N-adsorption with the extra atom (H, N, and O) decreased the critical temperature (τc) due to the reduction inEg1.
研究领域:
材料科学
·
光学工程
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DOI
高影响因子
Biomolecules
·
2026
·Vol. 16
·期 4
·609
·
IF 5.6
Xin Wang,Junlin Chen,Yimei Lai,Yumeng Wang,Kaixia Hu,Mengshi Wu,Niansheng Yang,Yuefang Huang
Macrophage-mediated inflammation is a key driver of sepsis-induced acute lung injury (ALI). M1 macrophage polarization relies on metabolic reprogramming, yet the upstream regulatory factors remain unclear. Lysine acetyltransferase 6A (KAT6A), a MYST-family acetyltransferase, regulates transcriptional programs in immune cells, but its role in macrophage function and ALI progression remains unknown. Public single-cell and bulk transcriptomic datasets were used to assess KAT6A expression changes and its association with inflammatory and metabolic pathways in macrophages. KAT6A inhibition with WM1119 was used to evaluate effects on M1 polarization, cytokine production, metabolic reprogramming, and PI3K-AKT-mTOR signaling. The therapeutic potential of KAT6A inhibition was validated in a cecal ligation and puncture (CLP)-induced sepsis model by assessing lung injury, bacterial clearance, and survival. KAT6A expression was upregulated in sepsis and particularly enriched in M1 macrophages. Inhibition of KAT6A reduced inflammatory and glycolytic transcriptional programs, suppressed glycolysis and enhanced oxidative phosphorylation, leading to decreased cytokine production and limited M1 polarization accompanied by suppression of PI3K-AKT-mTOR pathway. In CLP-induced septic mice, treatment with the KAT6A inhibitor WM1119 alleviated lung injury, improved bacterial clearance, and prolonged survival. KAT6A expression is associated with macrophage glucose metabolism, pro-inflammatory responses, and M1 macrophage polarization in sepsis-induced acute lung injury. Pharmacologic inhibition of KAT6A may provide a promising therapeutic strategy for reducing macrophage-driven lung injury.
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DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·Vol. 24
·期 1
·458
·
IF 15
Ma Yuxiao,Chen Guojie,Xu Pengcheng,Wang Baofeng,Teng Teng,Zheng Yongtao,Liu Yikui,Zhang Qixiang,Lai Tianqi,Wang Zhuohang,Sun Qingfang,Zhang Yongkang,Sun Yuhao,Bian Liuguan
Neuroinflammation mediated by microglia and excessive oxidative stress are key pathological processes driving the progression of brain injuries such as intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Modulating lactate transport has emerged as a promising approach to mitigate M1 microglia polarization and alleviate neuroinflammation. Liposomal nanoparticles provide a safe and efficient platform for drug delivery. Here, we developed reactive oxygen species (ROS) responsive MiRCM nanoparticles that co-deliver monocarboxylate transporter 1 (MCT1) inhibitor AR-C155858 and a ROS-scavenging PPS core, modified with CAQK and MG1 peptides for brain injury site and microglia targeting. MiRCM nanoparticles demonstrated ROS-induced degradation and controlled drug release, effectively protecting AR-C155858 from enzymatic degradation. In vitro and in vivo experiments exhibited that MiRCM nanoparticles selectively accumulated at injured brain regions and in M1-type microglia, where they scavenged ROS, inhibited lactate efflux, suppressed M1 microglia polarization and reduced inflammatory cytokine production in ICH and TBI models. Consequently, MiRCM treatment protected neurons, reduced astrocyte activation, preserved blood-brain barrier integrity, enhanced endogenous antioxidant enzyme activities, and alleviated neurological deficits in both ICH and TBI models. RNA sequencing further confirmed downregulation of inflammatory pathways. Moreover, biosafety evaluations revealed no significant histopathological or biochemical abnormalities in major organs, indicating good biocompatibility. In summary, this study offers a new MiRCM nanoparticle that effectively modulates lactate transport and eliminates ROS to suppress microglia M1 polarization and neuroinflammation, ultimately enhancing neural protection and functional recovery after ICH and TBI. Graphical The alternative text for this image may have been generated using AI. Schematic of MiRCM nanoparticles for ICH and TBI treatment
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DOI
高影响因子
Materials Today Bio
·
2025
·
IF 10.2
Weibei Sheng,Lin Li,Zimeng Zhou,Jin Zhao,Shaohua Ma,Yaohang Yue,Jian Weng,Ao Xiong,Deli Wang,Jianjing Lin,Hui Zeng,Peng Liu
The inflammatory microenvironment mediated by synovial macrophages, particularly the pro-inflammatory M1 subtype, plays a central role in OA progression and represents a critical therapeutic target. However, delivery strategies that enable efficient and selective targeting of M1 macrophages for modulating the inflammatory microenvironment are still limited. To address this challenge, we developed a glucose-functionalized nanoparticle system (Ber-MNPs) to deliver berberine directly to pro-inflammatory M1 subtype macrophages—via GLUT1-mediated targeting, thereby modulating the inflammatory microenvironment to alleviate OA progression. The Ber-MNPs exhibited excellent targeting specificity toward M1 macrophages in vitro . In addition, Ber-MNPs can suppress macrophage polarization toward the pro-inflammatory M1 phenotype, promote their transition to the anti-inflammatory M2 phenotype, and downregulate inflammatory cytokines, thereby protecting chondrocytes from catabolic damage. In a surgically induced OA mouse model, intra-articularly administered Ber-MNPs exhibited prolonged joint retention and mitigated OA progression by attenuating synovial inflammation and preserving cartilage integrity. Together, this study establishes a M1 macrophage-targeted nanotherapeutic platform that achieves precise inflammatory modulation, offering a new strategy for reshaping the synovial inflammatory microenvironment and achieving effective delay of OA progression
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产品关联
DOI
PubMed
高影响因子
FASEB JOURNAL
·
2025
·Vol. 39
·期 9
·e70561
·
IF 4.2
Haocong Zhang,Xianyun Qin,Hong Yuan,Liangbi Xiang,Hailong Yu
Neuronal inflammation and apoptosis aggravate the secondary injury after spinal cord injury (SCI). Cathepsin L (CTSL) is a lysosomal cysteine protease with effects on the regulation of inflammation, but its role in SCI remains unclear. The in vivo T10 mouse spinal cord contusion model was established. The results showed that CTSL expression was increased following SCI and then gradually decreased. Moreover, CTSL was mainly expressed in microglia. To detect the function of CTSL, after contusive injury, the mice were immediately injected with lentiviruses carrying CTSL shRNA. The results showed that CTSL depletion promoted functional recovery, accompanied by increased locomotor ability. CTSL deficiency reduced lesion cavity areas by inhibiting neuronal apoptosis and neuroinflammation. Indeed, CTSL deficiency decreased the secretion of TNF-α, IL-6, and MCP-1 and M1 microglia polarization in the spinal cord. CTSL depletion inhibited the expression and assembly of NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome. In vitro, CTSL expression was increased in LPS-treated BV2 cells. CTSL silencing repressed LPS-induced M1 polarization, as evidenced by the reduction in TNF-α, IL-6, and MCP-1 expression in the supernatant of BV2 cells. CTSL knockdown induced the downregulation of NLRP3 expression and activation. The inhibition role of CTSL knockdown in microglial inflammation and M1 polarization was reversed by NLRP3 agonist. Collectively, the study suggests that CTSL induces the microglia M1 polarization-mediated inflammation via promoting NLRP3 activation and thereby inhibits functional recovery after SCI. Graphical The inhibition of CTSL improves functional recovery and alleviates neuroinflammation through microglial polarization after spinal cord injury. Mechanically, CTSL knockdown inhibited NLRP3 expression and activation, which repressed the production of pro-inflammatory cytokines in M1 microglia, thereby inhibiting spinal cord injury-induced neuroinflammation.
研究领域:
神经科学
·
免疫学
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产品关联
DOI
PubMed
高影响因子
CELLULAR IMMUNOLOGY
·
2025
·
IF 2.9
Yiqi Wang,Xiuhua Zhang,Jiannan Zhang,Mingbo Zhao,Yang Chong,Quankuan Gu,Xianglin Meng,Mingyan Zhao
Acute lung injury (ALI) is a respiratory disease induced by uncontrolled inflammatory responses in the lungs. The pathological features of ALI include alveolar structural damage and pulmonary edema, which ultimately leads to pulmonary dysfunction. ANAPC5 (Anaphase-promoting complex subunit 5) is an E3 ubiquitin ligase known for its anti-inflammatory properties. This study aims to investigate the effects of ANAPC5 on ALI and its underlying molecular mechanism. In the lung tissue of an ALI mouse model induced by lipopolysaccharide (LPS) administration, we observed downregulation of ANAPC5. Through both in vivo and in vitro experiments, we assessed the effect of ANAPC5 on lung injury by conducting pathological analysis and molecular biological detection. ANAPC5 overexpression alleviated inflammatory cell infiltration, reduced alveolar wall thickening, suppressed pulmonary inflammation, and decreased the levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and lung tissue of the ALI model. Moreover, ANAPC5 inhibited M1 polarization and promoted M2 polarization of macrophages both in vitro and in vivo . We also found that ANAPC5 significantly suppressed the activation and expression of the epidermal growth factor receptor (EGFR) through inducing its ubiquitination in macrophages. In LPS-induced M1 macrophages, the presence of EGFR significantly decreased CD24 expression, followed by reversing the inhibitory effects of ANAPC5 on inflammatory responses and macrophage polarization. Collectively, our findings suggest that ANAPC5 serves as a therapeutic molecular target that mitigates ALI through regulating macrophage M1/M2 polarization via the EGFR/CD24 axis.
研究领域:
免疫学
·
呼吸病学
·
分子生物学
·
炎症反应调控
·
转化医学
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2026
·
IF 8.3
Chunyang Zhu,Fengyan Zhang,Xueni Li,Daijun Xing,Houhao Cai,Xinran Wang,Honglin Qu,Lisha Li,Xin Zheng
Background Non-small cell lung cancer (NSCLC), which constitutes approximately 85% of all lung cancer cases, is a leading cause of cancer mortality worldwide. Isoginkgetin (ISO), a biflavonoid isolated from Ginkgo biloba leaves, has demonstrated anticancer effects against various malignancies. However, its anti-NSCLC effects are unclear. Objective To explore the therapeutic potential of ISO and its mechanism of suppressing NSCLC proliferation. To provide experimental evidence for the translational potential of ISO as a candidate clinical drug. Methods Cell cytotoxicity and proliferation were assessed by cell viability, propidium iodide staining, colony formation, and cell cycle detection assays. Cell migration was evaluated by wound healing and transwell assays. Reactive oxygen species and the mitochondrial membrane potential were detected by fluorescent staining. Malondialdehyde and glutathione content were quantified by commercial assay kits. Transcriptome analysis for exploring the mechanism of ISO inhibition in NSCLC. The relationships between ISO and the tribbles pseudokinase 3 (TRIB3)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway were investigated through Western blot, siRNA-mediated TRIB3 knockdown, and overexpression of TRIB3. Cellular thermal shift assay and surface plasmon resonance were explored to investigate the binding and direct interaction between ISO and TRIB3. A non-contact co-culture model of NSCLC cells and macrophages was used to assess macrophage polarization. The anti-NSCLC effect of ISO in vivo was evaluated in a BALB/c nude mouse subcutaneous tumor model. Results ISO suppressed the cell viability, proliferation, and migration of NSCLC cells. ISO induces oxidative stress in NSCLC cells, characterized by an increase in reactive oxygen species and malondialdehyde and a decrease in mitochondrial membrane potential and glutathione. ISO has a strong binding affinity and direct interaction for the TRIB3 protein. Furthermore, ISO inhibited the antioxidant Nrf2 pathway by suppressing TRIB3 expression. Mechanistically, TRIB3 knockdown or overexpression significantly regulated the levels of oxidative stress and the Nrf2 pathway. ISO also promoted M1 macrophage polarization. Furthermore, ISO suppressed tumor growth in vivo . Conclusion ISO inhibits NSCLC through direct targeting and downregulation of TRIB3, thereby inducing oxidative stress and suppressing the antioxidant Nrf2 pathway. Furthermore, ISO regulates the tumor microenvironment by promoting M1 macrophage polarization. These findings may contribute to improved prognosis for NSCLC patients and provide insights into the mechanism of ISO as an antitumor drug, thereby supporting its potential for clinical translation.
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·Vol. 24
·期 1
·361
·
IF 15
Wang Yanyi,Ren Jiangyan,Ren Tingyu,Li Baochao,Ran Jianchuan,Wang Huijuan,Huang Ziwei,Xie Diya,Liu Tao,Yang Linzhong,Zhang Jinglun,Zhang Caixia,Wang Zhi,Luo Xingyu,Zheng Lei,Xie Xiaoji,Li Huang,Han Wei
Temporomandibular joint osteoarthritis (TMJOA) involves progressive synovial inflammation-driven cartilage degeneration. While thermotherapy empirically alleviates symptoms, its immunomodulatory mechanism remains elucidated. Here, we revealed that targeted mild hyperthermia reprogramed synovial M1 macrophages via NF-κB pathway suppression, shifting their secretome to attenuate chondrocyte catabolism while enhancing anabolism. This thermally-modified macrophage conditioned medium concurrently promoted osteogenic mineralization. Capitalizing on this, we engineered folic acid-conjugated Y8 nanocomposites (FA-Y8 NPs) for precision M1-targeting photothermal therapy. Under 808 nm irradiation, FA-Y8 NPs achieved localized photothermal reprogramming of synovial M1 macrophages and attenuating cartilage degradation in CFA-induced TMJOA mice. This study reveals thermal immunomodulation of synovial macrophages as a potential mechanism for TMJOA remission and establishes a targeted nanoplatform for spatial control of joint inflammation. Graphical The alternative text for this image may have been generated using AI.
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DOI
PubMed
高影响因子
BIOMATERIALS
·
2024
·
IF 12.8
Fuhong Yang,Jingqi Lv,Yanli Huang,Wen Ma,Zhen Yang
As regulators and promotors of joint erosion, pro-inflammatory M1-like macrophages play pivotal roles in the pathogenesis of rheumatoid arthritis (RA). Here, we develop a supramolecular self-assembly (PCSN@MTX) of molybdenum (Mo) based polyoxometalate (POM), β-cyclodextrin (β-CD), and methotrexate (MTX), in which the MTX is loaded by host-guest interaction. PCSN@MTX shows inhibition of synovial M1-like macrophages polarization to alleviate RA. PCSN@MTX has demonstrated ultrasound (US) augmented catalytic behavior in consuming ROS and generating oxygen (O 2 ) with accelerated conversion of Mo 5+ to Mo 6+ in the POM. In the collagen-induced arthritis mouse model, after systemical administration, the pH-responsive PCSN@MTX shows enhanced accumulation in the acidic joints by in-situ self-assembly. The host-guest complexation between MTX and β-CD is broken via US, achieving an on-demand burst release of MTX. The released MTX and ROS-scavenging synergistically facilitate the M1-to-M2 macrophage phenotype switching, which effectively alleviates RA disease progress under US irradiation. This study provides a paradigm for RA therapy with a promising US-augmented strategy.
研究领域:
药理学
·
风湿病学
·
纳米医学
·
炎症研究
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DOI
PubMed
高影响因子
Nanoscale
·
2020
·Vol. 12
·期 16
·8664-8678
·
IF 6.895
Xin Chang,Lei Xing,Yi Wang,Tian-Jiao Zhou,Li-Jun Shen,Hu-Lin Jiang
Effective treatment in clinic for idiopathic pulmonary fibrosis (IPF) remains a challenge due to low drug accumulation in lungs and imbalanced polarization of pro/anti-inflammatory macrophages (M1/M2 macrophages). Herein, a novel endogenous cell-targeting nanoplatform (PNCE) is developed for enhanced IPF treatment efficacy through modulating M1/M2 macrophages into the balanced status to suppress fibroblast over-activation. Notably, PNCE loaded with nintedanib (NIN) and colchicine (COL) can firstly target endogenous monocyte-derived multipotent cells (MOMCs) and then be effectively delivered into IPF lungs due to the homing ability of MOMCs, and detached sensitively from MOMCs by matrix metalloproteinases-2 (MMP-2) over-expressed in IPF lungs. After PNCE selectively accumulated within fibrosis foci, COL can mildly modulate the polarization of M1 macrophages into M2 macrophages to balance innate immune responses, which can enhance the suppressing effect of NIN on fibroblast activation, further improving the IPF therapy. Altogether, PNCE has two collaborative steps including the inhibition of innate immune responses accompanied by the decrease of fibroblast populations in IPF lungs, achieving a stronger and excellent anti-fibrotic efficacy both in vitro and in vivo. This endogenous cell-based engineered liposomal nanoplatform not only allows therapeutic drugs to take effect selectively in vivo, but also provides an alternative strategy for an enhanced curative effect by modulating innate immune responses in IPF therapy.
研究领域:
药理学
·
纳米技术
·
免疫学
·
肺科学
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DOI
PubMed
高影响因子
MEDIATORS OF INFLAMMATION
·
2023
·
IF 4.6
Zhousheng Yang,Tianyu Li,Chunyan Wang,Mingyu Meng,Shenglan Tan,Lei Chen
Dihydromyricetin (DMY), a natural flavonoid compound extracted from the stems and leaves of Ampelopsis grossedentata, has been found as a potential therapeutic chemical for treating atherosclerosis. This study explores the underlying mechanism of DMY repressing M1 macrophage polarization in atherosclerosis. We showed that DMY treatment markedly decreased M1 macrophage markers (e.g., Tnf-α and IL-1β) and p65-positive macrophage numbers in the vessel wall of Apoe-deficient (Apoe–/–) mice. Overexpression of miR-9 or knockdown of SIRT1 in macrophages reversed the effect of DMY on M1 macrophage polarization. The data we presented in the study indicate that the miR-9-mediated SIRT1/NF-κB pathway plays a pivotal role in M1 macrophage polarization and is one of the molecular mechanisms underlying the anti-atherosclerosis effects of DMY. We provide new solid evidence that DMY may be explored as a potential therapeutic adjuvant for treating atherosclerosis.
研究领域:
药理学
·
免疫学
·
心血管疾病
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DOI
PubMed
高影响因子
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