Advanced Healthcare Materials
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2025
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IF 9.6
Yanxue Si,Ruitao Cha,Pai Zhang,Fengshan Zhou,Wenbing Yuan,Xingyu Jiang
5-Aminosalicylic acid (5-ASA) is the first-line drug for ulcerative colitis (UC), which encounters therapeutic constraints due to the poor water solubility and absorption by the upper gastrointestinal. Here, a cyclodextrin-based metal-organic framework (CD-MOF) is used as a carrier for 5-ASA (ASA@CM) to enhance its solubility. To improve the targeted release 5-ASA, ASA@CM is incorporated into sodium alginate/ L -arginine complex (SA-LA) to obtain the desired microspheres (ASA@CM/SL) by electrospray. ASA@CM/SL safeguards 5-ASA against the harsh gastrointestinal environment and provides favorable delivery to the colon. The anti-inflammatory and anti-oxidant activity is studied by measuring inflammatory factors and reactive oxygen species (ROS). The therapeutic effect of ASA@CM/SL on UC mice induced with dextran sulfate sodium is assessed. The biosafety by evaluating cytotoxicity and organ toxicity is studied. ASA@CM/SL shows excellent therapeutic effects for UC, as evidenced by its alleviation of inflammatory response and restoration of disrupted intestinal barriers. ASA@CM/SL features low cytotoxicity and low organ toxicity. This study provides a potential strategy for improving 5-ASA solubility and delivery efficiency, which may also be applied to broadly tackle various small hydrophobic molecules to treat UC and other intestinal diseases.
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Materials Today Chemistry
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2025
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IF 6.7
Rui Zhang,Meilan Liu,Lin Bao,Huanchen Yan,Huahui Feng,Danyi Huang,Ying Ding,Min Chen
Chondrodysplasia presents with abnormal chondrocyte differentiation and altered cartilage extracellular matrix, which restricts cartilage and bone growth. Kartogenin (KGN) is recognized as a chondroinductive molecule, whereas the limitation of hydrophobicity and low bioavailability are obstacles to therapy. Nanocarriers for drug delivery can potentially defeat some of the challenges of drug delivery of hydrophobic species. Herein, ROS-responsive core-shell codelivery nanocarriers were developed for chondrogenesis with a core consisting of mesoporous silica nanoparticles (MSN) loaded with KGN and embedded with ultrasmall Prussian blue (USPB), and a shell consisting of selenized hyaluronic acid (Se-HA). MKP@Se-HA nanoparticles effectively improved the bioavailability of KGN. The embedded USPB enhanced structural stability and antioxidant properties, while Se-HA coating targeted chondrocytes via CD44 and employed diselenide bonds as ROS-responsive to achieve KGN release at lesion sites. In vitro and in vivo experiments demonstrated that MKP@Se-HA nanoparticles could promote chondrocyte proliferation and differentiation by upregulating SOX9 and Col II expression. Meanwhile, MKP@Se-HA nanoparticles had a positive effect in the zebrafish chondrodysplasia model by modulating the formation of cartilage matrix and reducing apoptotic cells. Overall, the prepared core-shell codelivery nanoparticles offer a promising strategy for improving chondrodysplasia by synergistically promoting chondrocyte proliferation and differentiation.
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TOXICOLOGY
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2026
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IF 4.6
Jin Chen,Hanwen Hu,Jing Fu,Yaolin He,Hui Zhou,Jingwei Lei,Ming Huang,Jianqi Wang,Anfei Liu,Zhenzhong Liu
Trimethyltin chloride (TMT), a pervasive environmental organic tin pollutant, has been implicated in cardiac injury, though its underlying mechanisms remain unclear. TMT exposure triggers excessive reactive oxygen species (ROS) generation, a key inducer of ferroptosis—a regulated form of cell death driven by iron-dependent lipid peroxidation. NADPH oxidase 4 (NOX4), highly expressed during cardiac development, plays a critical role in myocardial ROS production, while the Keap1/Nrf2 pathway regulates cellular ROS homeostasis. We hypothesized that TMT induces cardiac developmental defects by activating NOX4/Keap1/ROS-mediated ferroptosis. TMT exposure induced cardiac malformations, pericardial edema, and reduced heart rate in zebrafish embryos. Further studies revealed that TMT upregulated nox4 expression in embryonic hearts. Notably, pharmacological inhibition or genetic knockdown of nox4 markedly attenuated TMT-induced cardiac defects. Moreover, nox4 suppression antagonized TMT-triggered dysregulation of the Keap1/Nrf2 axis, ROS overaccumulation, mitochondrial damage, and ferroptosis-related abnormalities—including Fe²⁺ accumulation, elevated lipid peroxidation, and downregulated glutathione peroxidase 4 (GPX4) expression. Crucially, inhibition or knockdown of keap1 similarly mitigated TMT-induced ROS bursts, mitochondrial injury, and ferroptosis progression. Intervention with ferroptosis-specific inhibitors (Liproxstatin-1 and Myricetin) confirmed that ferroptosis directly contributes to TMT-induced cardiac developmental defects. This study demonstrates that TMT induces cardiac malformations by activating ferroptosis via the nox4/Keap1/Nrf2/ROS signaling axis. These findings reveal a novel mechanism underlying TMT cardiotoxicity, provide theoretical insights for assessing TMT exposure as a risk factor for congenital heart disease, and identify potential molecular targets for therapeutic intervention.
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Materials Today Bio
·
2026
·
IF 10.2
Lihang Qu,Tu Lu,Jun Tan,Xinzhao Chen,Tian Tian,Shixiang Liu,Yajun Gong,Zhihao Jiang,Zhonggui He,Peng Sun,Jin Sun,Xiaoli Ma,Ruidong Gu
Choroidoretinopathy is a major public health concern that causes significant vision impairment. Although therapeutic antibodies have demonstrated potential in treating these conditions, intravitreal injections remain invasive, associated with adverse effects, and require repeated traumatic administrations. Non-invasive drug delivery methods, such as eye drops, represent an ideal alternative but are limited by ocular barriers, making it difficult for drugs to effectively reach specific lesions. In this study, we introduce a novel reactive oxygen species (ROS)-responsive transmembrane peptide–antibody conjugate (PAC) designed for non-invasive, precise antibody delivery to the deep fundus region. The responsive PAC, termed trans-activator of transcription–polyethylene glycol–maleimide (TAT-MPEG)-antibody, is synthesized by linking transmembrane peptides TAT to maleimide via ROS-sensitive diselenide bonds, enabling efficient antibody conjugation. Following eye drop administration, TAT enhances ocular penetration, allowing the conjugate to traverse ocular barriers and deliver antibodies directly to the posterior segment. Moreover, the diselenide bonds facilitate antibody release in oxidative environments, ensuring targeted drug localization at disease sites. In mouse models of choroidal neovascularization and choroidal melanoma, this conjugate demonstrated significant therapeutic efficacy, highlighting its broad clinical potential for the treatment of choroidoretinopathy.
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CHEMICAL ENGINEERING JOURNAL
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2026
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IF 12.5
Zijian Wang,Wei Jin,Ying Zhou,Jieying Zhang,Xinkun Shen,Caiyun Mu,Maowen Chen
A bioresponsive multifunctional composite system is constituted by the HHPP hydrogel, which integrates PBA-OHA and PVA with composite nanoparticles (RB-HNTs). • For the first time, regaloside B (RB) within the hydrogel is found to exert anti-inflammatory effects through inhibition of the AGE-RAGE signaling pathway. • By combining RB and bioactive silicon, the hydrogel restores mitochondrial membrane potential and enhances the osteogenic differentiation of BMSCs. • In vivo, the hydrogel accelerates diabetic bone defect healing by alleviating ROS-induced inflammation and promoting osteogenesis. Repairing diabetic bone defects remains challenging due to hyperglycemia, oxidative stress, chronic inflammation, and metabolic dysfunction. To address this, we developed a bioresponsive multifunctional composite hydrogel (HHPP) based on phenylboronic acid-modified oxidized hyaluronic acid (OHA-PBA) and polyvinyl alcohol (PVA), encapsulating composite nanoparticles (RB-HNTs). In the diabetic microenvironment, regaloside B (RB) released from the hydrogel scavenges reactive oxygen species (ROS), promotes M1-to-M2 macrophage polarization, and alleviates inflammation. Network pharmacology and western blotting revealed that this anti-inflammatory effect is associated with the AGE-RAGE signaling pathway. RB also restores mitochondrial function and reverses metabolic disorders in bone marrow mesenchymal stem cells (BMSCs) under diabetic conditions, while synergizing with bioactive silicon released from HNTs to enhance BMSC osteogenesis. In vivo, HHPP significantly reduces glucose-ROS-induced inflammation and promotes bone formation, accelerating diabetic bone defect healing. This study offers a viable strategy for treating diabetic bone defects. Schematic illustration of the fabrication of HHPP hydrogel and its application. Download: Download high-res image (165KB) Download: Download full-size image
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ENVIRONMENT INTERNATIONAL
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2026
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IF 10.2
Xingcheng Li,Xiao Li,Cimei Li,Lingfen Cao,Siteng Li,Xiaoping Wang,Kangchao Du,Yaoyao Cui,Yuxiang Ma,Xu Wang,Xing Xing,Huigen Feng,Ciqing Yang,Xianwei Wang,Cixia Li
PFOA and GenX disrupt adult hippocampal neurogenesis and synaptic remodeling. • PFAS exposure alters anxiety-related behaviors and spatial learning–memory performance in mice. • PFOA preferentially reduces PSD95, whereas GenX preferentially reduces synaptophysin expression. • PFOA and GenX increase microglial abundance and induce reactive morphological changes in the hippocampus. • PFAS exposure is associated with oxidative stress and ferroptosis-related molecular alterations in the hippocampus. Per- and polyfluoroalkyl substances (PFAS) accumulate in the hippocampus, yet their effects on adult hippocampal neurogenesis (AHN) remain unclear. In this study, adult male mice were orally exposed to PFOA or GenX (2 or 10 mg/kg/day) for 28 days. Behavioral performance, AHN, synaptic remodeling, microglial morphology, and redox status were evaluated using behavioral assays, Nissl and Golgi staining, BrdU immunolabeling, microglial morphometric analyses, and Western blotting. PFOA exposure and high-dose GenX exposure reduced time spent and distance traveled in the center area of the open field and impaired spatial learning and memory performance in the Morris water maze, as indicated by increased escape latency and fewer platform crossings. In contrast, PFOA and low-dose GenX exposure reduced exploration of the open arms in the elevated plus maze. PFOA and GenX reduced dendritic spine density with fewer mushroom/thin spines and more stubby spines. PFOA preferentially decreased PSD95 (postsynaptic marker), whereas GenX reduced synaptophysin (presynaptic marker). In the subgranular zone (SGZ), survival and neuronal differentiation of neural stem cells were diminished, and asymmetric divisions of radial glia-like cells increased, suggesting stem-cell pool depletion. Microglia exhibited a hyper-ramified/bushy reactive phenotype. Hippocampal ROS/MDA rose, NOX2 components (GP91 phox /P22 phox ) were upregulated, and ferroptosis defenses (SLC7A11/GLS2/GPX4) were downregulated. Collectively, PFOA and GenX disrupt hippocampal synaptic remodeling and AHN and are associated with increased oxidative stress and ferroptosis-related alterations. Differential pre- versus postsynaptic vulnerabilities may contribute to the distinct behavioral alterations observed following PFOA and GenX exposure. This work provides new insights into the neurotoxic effects of PFOA and GenX and identifies potential pathways involved in PFAS-induced hippocampal dysfunction. Download: Download high-res image (180KB) Download: Download full-size image
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Science Advances
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2025
·Vol. 11
·期 44
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IF 12.5
Ganghua Yang,Jianqiu Yang,Zhaoping Diao,Jiajun Long,Zhiwen Shu,Chengkang Liu,Wenbing Wan
Precise macrophage modulation is essential for diabetic wound treatment, yet mitochondrial dysfunction often sustains proinflammatory states. We developed cascade-targeting nanoparticles [epigallocatechin-3-gallate and metformin nanoparticles modified with mannose (EM/Man NPs)] to regulate macrophage mitochondria, integrated into a detachable core-shell microneedle patch (EM/Man MNs) made of quaternary ammonium chitosan and reactive oxygen species (ROS)–degradable polymer. The patch offered high penetration and antibacterial activity, while its ROS-sensitive core released EM/Man NPs to scavenge ROS, restore adenosine 5′-triphosphate production, and reestablish redox balance. The NPs further activated the adenosine 5′-monophosphate–activated protein kinase/Sirtuin 1/peroxisome proliferator–activated receptor gamma coactivator 1α axis to promote mitochondrial biogenesis and oxidative phosphorylation, repolarizing macrophages to an anti-inflammatory phenotype. In diabetic mice, EM/Man MNs accelerated healing via bacterial clearance, immune reprogramming, angiogenesis, and collagen deposition while inhibiting scar formation through interleukin-17 and phosphatidylinositol 3-kinase–Akt suppression. This cascade-targeting strategy for modulating macrophage mitochondria to regulate immunity and redox homeostasis provides a previously unidentified approach for designing tissue engineering materials.
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ACS Applied Polymer Materials
·
2025
·
IF 4.7
Ya Hu,Lin Xiao,Mingwen Zang,Jinhong Zhang,Yan Jiang,Yi Zhang,Liuya Wei,Jibin Wang,Zhicui Liu,Junhui Zhao
Herein, we present an infection microenvironment (IME)-adaptive covalent organic framework (COF), termed Cu–B–COF, engineered through dynamic assembly of a bidentate N-substituted salicylimine-Cu complex [Cu(SALANIH-boronic acid)2] and 5,10,15,20-tetrakis(2,3-dihydroxyphenyl)porphyrin. Cu–B–COF, integrating the characteristics of both metal–organic frameworks (MOFs) and COFs, could be used as a therapeutic agent for infectious wound healing. This intelligent platform features pH/H2O2-responsive boronate esters, enabling structural reconfiguration, followed by size switching and biodegradability. The Cu-based catalytic centers enable glutathione peroxidase-like (GPx-like) and peroxidase-like (POD-like) activities. Notably, the bidentate salicylimine-Cu units induce a spatial twisted three-dimensional structure, allowing efficient utilization of light energy, promoting both photothermal conversion and photodynamic processes while minimizing losses due to aggregation-induced quenching. As a result, Cu–B–COF exhibits superior photothermal conversion efficiency compared to its porphyrin precursor, while simultaneously demonstrating dual-modal photodynamic capabilities (Type I/II mechanisms), enabling self-adapting therapeutic cascades through three distinct operational phases. The synergistic glutathione (GSH) depletion and photothermal-potentiated POD-mimetic cycling cooperatively amplify hydroxyl radical (•OH) burst and ROS storm generation, enabling deep-tissue pathogen elimination through enhanced catalytic penetration. Subsequent acid neutralization (via H+ consumption) and H2O2 scavenging mechanisms concertedly reconstruct a regenerative niche, restoring physiological pH homeostasis while eliminating oxidative stress barriers. Sustained Cu2+ release drives neoangiogenesis, while antioxidant polyhydroxyl orchestrates matrix reconstruction and epithelial migration. This multiscale engineering strategy overcomes critical limitations of conventional enzyme therapies, including insufficient ROS yield in hypoxic microenvironments, self-limiting catalytic efficiency, and deficient vascular support during tissue remodeling.
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BIOMATERIALS
·
2025
·
IF 12.9
Lamei Liu,Min Zhang,Yan Zhou,Lin He,Mingjian Chen,Yuchen Wu,Guanyu Yin,Hui He,Lanlin Qi,Bin Zhang,Xiaoxiao He,Kemin Wang
Osteoarthritis (OA) is a complex and multifactorial joint disorder. Currently, there are few therapies to slow the progression of OA. Combining symptomatic slow-acting drugs and reactive oxygen species (ROS) scavenging reagents in the inflamed joint shows a promising therapeutic approach for OA. Nonetheless, the short residence time of free drugs in the joint cavity hinders their further application. Herein, an injectable composite of hydrogel and chondroitin sulfate@resveratrol liposome package (Gel/Lip@Res + Chs) was developed to improve drug residency ability and enable the simultaneous delivery of hydrophilic Chs and hydrophobic Res in the joint cavity. This injectable hydrogel, based on phenylboronic acid modified hyaluronic acid (HAPBA) and polyvinyl alcohol (PVA), provided ROS-responsive decomposition property and sustained drug release behavior, thereby effectively scavenging ROS, promoting macrophage repolarization, and decreasing the expression of inflammatory mediators and matrix-degrading enzymes in vitro . As a proof of concept, the in vivo therapeutic efficacy of Gel/Lip@Res + Chs was further examined in both monoiodoacetic acid (MIA)-induced and surgical anterior cruciate ligament transection (ACLT)-induced OA mouse models. Benefiting from the extended residence time of loaded drugs in the joint cavity, the Gel/Lip@Res + Chs treatment could effectively suppress cartilage degeneration and increase the synthesis of the cartilage matrix, thus slowing the advancement of OA. The present study provides a reference for improving drug retention and holds great potential for treating OA-related diseases.
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MATERIALS & DESIGN
·
2025
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IF 7.9
Ziming Wang,Yi Wang,Mengxue Hou,Qinghai Liu,Mengting Zhang,Lei Ge,Junfeng Gao,Feng Sun,Qingqing Guan,Tao Jiang,Chunhua Geng,Pinping Jiang,Yunxin Ge,Jie Shan,Jianghao Xing,Hongxia Li
Radiation pneumonitis (RP), a major dose-limiting toxicity of thoracic radiotherapy, is primarily driven by excessive reactive oxygen species (ROS) accumulation and proinflammatory macrophage activation, yet effective therapeutic strategies remain unavailable. Herein, we constructed Ti 3 CN nanosheets (Ti 3 CN NSs) via HF etching followed by ultrasonic exfoliation, enabling potent catalytic ROS scavenging and immunomodulatory activities. Leveraging their intrinsic antioxidative properties, Ti 3 CN NSs were systematically evaluated across cell, mice, and lung organoid models, demonstrating robust elimination of radiation-induced ROS and restoration of pulmonary redox homeostasis. Transcriptome sequencing combined with pathway enrichment analysis revealed that Ti 3 CN NSs alleviated radiation-induced macrophage ferroptosis, thereby rebalancing macrophage polarization by suppressing M1 and promoting M2 polarization. In vivo , Ti 3 CN NSs attenuated RP progression and facilitated structural repair of injured lung tissue. Collectively, this work proposes a nanomaterial-based strategy for the prevention and treatment of RP, and highlights the critical roles of macrophage polarization and ferroptosis in radiation-induced pulmonary inflammation.
研究领域:
纳米医学
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放射肿瘤学
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炎症生物学
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氧化还原生物学
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免疫调节
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ACS Applied Engineering Materials
·
2025
·
IF 3.5
Mengzhu Xiao,Yujia Wu,Wanzhen Li,Jun Wang,Weiwei Zhang,Zuchun Zhao,Fei Ge
The overuse of antibiotics leads to bacterial resistance, which involves complex and diverse mechanisms, among which the activation of drug efflux pumps is a key contributing factor. Excessive accumulation of reactive oxygen species (ROS) in inflamed wound tissues further exacerbates this issue by triggering efflux pump activation. To address bacterial resistance, this study aimed to mitigate ROS accumulation, thereby inhibiting efflux pump expression and enhancing antibacterial efficacy. Researchers synthesized MoS2-based nanocomposites (MoS2/ZnO/Cur designated as MZCs) loaded with ZnO and Cur into cross-linked structures using a hydrothermal method and combined them with photothermal therapy (PTT). To enhance functionality, a ROS-responsive hydrogel was developed by conjugating CGG with a ROS-responsive linker (TPA) and integrating the MZCs, yielding MZC@CGG-TPA. Electron microscopy revealed the internal structure of the hydrogel. Antibacterial assays demonstrated that MZC@CGG-TPA achieved inhibition rates exceeding 95% against multidrug-resistant (MDR) Escherichia coli and Staphylococcus aureus, with biofilm clearance rates surpassing 90%. Photothermal performance testing indicated a photothermal conversion efficiency of 47%. Transcriptomic analysis revealed that MZC@CGG-TPA suppressed the expression of channel protein-related genes, downregulated the key regulator gene marA, and inhibited drug efflux pump activity. This enhanced the retention of antibacterial agents within bacterial cells and improved bactericidal efficacy. Under laser irradiation, the MZC@CGG-TPA hydrogel dressing significantly enhanced anti-infection efficacy and accelerated wound healing in an in vivo wound infection model. These findings present an approach for designing advanced nanosystems to effectively combat MDR bacteria.
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Advanced Materials Interfaces
·
2023
·
IF 5.4
Lin Duan,Yanyan He,Haigang Wu,Tianxiao Li,Jia Liang,Rufeng Jia,Dehua Guo,Taoyuan Lu,Chi Ma,Wenbo Liu,Yingkun He
Nitinol (NiTi) alloy is an ideal material for preparing neurointerventional stents due to its excellent mechanical properties and biocompatibility. However, NiTi stents without surface-specific functionalization cause a high rate of stent thrombosis and in-stent restenosis after implantation. In ischemic stroke, exosomes have a role in regulating nervous system development, regeneration, vascular remodeling, and neuroinflammation. In this work, the effect of exosome coating on the biocompatibility of NiTi alloy is evaluated. NiTi alloy is successively immersed in relevant solution (sodium alginate, 3-aminophenylboronic acid, distearoylphosphatidylethanolamine, and exosomes) to form ROS-responsive exosome coated surfaces. In vitro experiments (platelets, endothelial cells, smooth muscle cells, and macrophages) and in vivo subcutaneous implantation experiments are performed to test coatings for biocompatibility. The results show that the modified NiTi alloy surface has high hydrophilicity, which has the functions of inhibiting platelet aggregation, promoting endothelialization, inhibiting smooth muscle cell migration, anti-inflammatory, and good tissue biocompatibility. This study develops exosome neurointerventional stent coating as a bioactive drug via reactive oxygen species accumulation in lesions, thus targeting drug release, inhibiting intimal hyperplasia, and reducing inflammation and thrombosis.
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