JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION
·
2025
·
IF 3.6
Zeyue Sun,Xiaojun Li,Xueheng Sun,Liuting Chen,Zihang Wang,Xin Feng,Luying Wang,Wenjie Jin,Xin Sun,Jiaju Lu
Bone regeneration is frequently impaired by excessive reactive oxygen species (ROS) and prolonged inflammation, which disrupt the immune microenvironment and hinder osteogenesis. The stimulator of interferon gene (STING) pathway is an innate immune pathway and a critical mediator of the inflammatory response, has been increasingly implicated in inflammatory bone loss and impaired repair. While STING inhibition represents a promising therapeutic strategy, its effective implementation within the bone microenvironment requires spatiotemporally controlled delivery. Here, we developed an injectable and photocrosslinkable hydrogel system (GMPP+H151) that integrates ROS-responsive scavenging with targeted STING inhibition to synergistically guide immune microenvironment remodeling and bone regeneration. The GMPP hydrogel was fabricated through dual crosslinking of phenylboronic acid (PBA)-modified gelatin (GelMA) and polyvinyl alcohol (PVA), endowing it with self-healing properties and ROS-scavenging capacity. H151, a small molecule inhibitor of STING, was caged by PBA chemistry for on-demand release under oxidative stress. The GMPP+H151 can significantly reduce ROS levels in macrophages and promote their phenotypic differentiation from M1 to M2 by suppressing the STING pathway, downregulating pro-inflammatory cytokines, and upregulating anti-inflammatory factors. Furthermore, it efficiently enhanced survival, spreading, and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), leading to increased expression of alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX2), and osteocalcin (OCN). This study presents a smart, multifunctional hydrogel drug delivery system that integrates immunomodulation and osteoinduction, offering a promising strategy for promoting osteogenic differentiation and in situ bone defect repair.
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高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Yongcen Chen,Xuemin Ma,Yajuan Hu,Huiyue Wang,Peirong Zhou,Xiaoping Tian,Haofeng Wang,Yun He,Gang Tao,Rui Cai,Junliang Chen
Diabetic wounds are marked by persistent infection, hypoxia, excessive reactive oxygen species (ROS), and impaired angiogenesis, which present significant challenges for clinical management. In this study, a pH/ROS dual-responsive multifunctional hydrogel (QOF-EGCG/Hb@PDA) was constructed by grafting 3-carboxyl-4-ffuorophenylboronic acid (FPBA) onto Quaternary ammonium chitosan (QCS) to form Schiff base bonds with Oxidized gellan gum (OGG) (pH response), and by reacting FPBA with Epigallocatechin gallate (EGCG) to form borate bonds (ROS response). Hb@PDA nanoparticles were then loaded into the hydrogel. Under acidic conditions, the cleavage of Schiff base bonds triggers the release of Hb@PDA, providing sustained oxygen delivery to alleviate hypoxia. Additionally, in ROS-rich environments, the cleavage of borate ester bonds promotes EGCG release, exerting antioxidant and anti-inflammatory effects. QOF-EGCG/Hb@PDA displays excellent self-healing capacity and tissue adhesion, as well as remarkable photothermal activity. Furthermore, it demonstrates excellent antibacterial, antioxidant, anti-inflammatory, pro-angiogenic, and hemostatic properties. In vivo studies confirmed that this hydrogel markedly accelerated diabetic wound healing by enhancing epithelial regeneration, promoting collagen deposition, regulating inflammatory responses, and facilitating angiogenesis. Transcriptomic analysis revealed that the hydrogel promotes angiogenesis by activating the HIF-1α/VEGF signaling pathway, which plays a pivotal role in vascular formation and tissue regeneration, thereby accelerating the healing of diabetic wounds. Collectively, QOF-EGCG/Hb@PDA provides a promising and comprehensive strategy with great potential for application in diabetic wound treatment.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2024
·Vol. 22
·期 1
·1-21
·
IF 10.6
Li Fupeng,Mao Zhiyuan,Du Yun,Cui Yuehan,Yang Shengbing,Huang Kai,Yang Jian,Li Zhuoyuan,Liu Yihao,Gu Jinlou,Wang Danru,Wang Chen
Excessive production of reactive oxygen species (ROS) and inflammation are the key problems that impede diabetic wound healing. In particular, dressings with ROS scavenging capacity play a crucial role in the process of chronic wound healing. Herein, Zr-based large-pore mesoporous metal–organic frameworks (mesoMOFs) were successfully developed for the construction of spatially organized cascade bioreactors. Natural superoxide dismutase (SOD) and an artificial enzyme were spatially organized in these hierarchical mesoMOFs, forming a cascade antioxidant defense system, and presenting efficient intracellular and extracellular ROS scavenging performance. In vivo experiments demonstrated that the SOD@HMUiO-MnTCPP nanoparticles (S@M@H NPs) significantly accelerated diabetic wound healing. Transcriptomic and western blot results further indicated that the nanocomposite could inhibit fibroblast senescence and ferroptosis as well as the stimulator of interferon genes (STING) signaling pathway activation in macrophages mediated by mitochondrial oxidative stress through ROS elimination. Thus, the biomimetic multi-enzyme cascade catalytic system with spatial ordering demonstrated a high potential for diabetic wound healing, where senescence, ferroptosis, and STING signaling pathways may be potential targets. Graphical Abstract
Schematic diagram showing the proposed mechanism that S@M@H NPs promoted diabetic wound healing
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高影响因子
ACS Applied Materials & Interfaces
·
2025
·
IF 8.2
Chenyu Ma,Wen Ding,Peiting Li,Qiyue Wang,Xueming Li,Zhengjie Meng,Hao Ren
Macrophage dysregulation and microbial dysbiosis at diabetic chronic wound sites are two of the main drivers that hinder the healing process. To address this, a reactive oxygen species (ROS)-responsive hydrogel wound dressing (NVs@CO-TP) is fabricated through boronic ester bonds between poly(vinyl alcohol) hydroxyl groups and phenylboronic acid moieties, which incorporates M2 macrophage-derived nanovesicles (NVs) loaded with manganese carbonyl (NVs@CO). Upon exposure to a high level of ROS in the wound, the hydrogel responds, scavenges ROS, and subsequently releases NVs@CO, exhibiting the synergistic efficacy of CO gas and NVs. Due to its intrinsic inflammation-tendency ability, NVs@CO specifically targets activated M1 macrophages and releases CO to regulate mitochondrial metabolism, promoting M1 apoptosis and increasing the M2 phenotype. This process decreases the release of inflammatory cytokines and enhances anti-inflammatory processes, promoting chronic diabetic wound healing. More interestingly, the dressing also beneficially modulates the wound microbiota by enhancing the beneficial microbial richness and overall microbiome composition, which further improves the healing microenvironment. Therefore, NVs@CO-TP acts through two primary mechanisms: the targeted delivery of CO to M1 macrophages regulates the mitochondrial metabolism to repolarize macrophages while simultaneously modulating the wound microbiome. This combined anti-inflammatory strategy facilitates chronic wound healing and demonstrates significant potential for clinical translation in treating various difficult-to-heal wounds.
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EUROPEAN POLYMER JOURNAL
·
2026
·
IF 6.8
Zhen Xu,Guo Chen,Zhinan Ren,Jiansen Wang,Kaixu Han,Yukang Qin,Dongfeng Li,Lei Yu,Guangduo Zhu,Longqing Li,Yingjie Hao,Cheng Peng
Excessive ROS create a chronic inflammatory microenvironment in diabetic wounds, while hyperglycemia promotes bacterial infection, together driving a vicious cycle of tissue damage. In this study, a cerium–tannic acid coordinated metal–polyphenolic network (Ce@PTA MPN) was developed to scavenge ROS at the wound site. This complex was subsequently integrated into a phenylboronic acid-modified methacrylated hyaluronic acid–PEG hybrid hydrogel, designed as a functional wound dressing. The Ce@PTA MPN exhibited efficient ROS-scavenging ability via catalytic activity. Additionally, the photo-crosslinked hybrid hydrogel demonstrated favorable mechanical properties, including tensile strength and self-healing capability. Notably, the Ce@PTA complex was released in response to oxidative stimuli due to the reversible phenylboronic ester linkage between tannic acid and the modified hydrogel (b-Gel), which enhanced antioxidant, antibacterial and anti-inflammatory efficacies while minimizing potential cytotoxicity. In animal experiments, Ce@PTA b-Gel accelerated skin defect repair by inhibiting bacterial proliferation and promoting epidermal regeneration. The expression of pro-inflammatory cytokines was reduced, while CD31 expression was increased in the regenerated skin. Transcriptomic analysis revealed that the therapeutic mechanism of Ce@PTA b-Gel involved the dual suppression of inflammatory signaling and restoration of metabolic homeostasis. Collectively, Ce@PTA b-Gel may represent a potential therapeutic strategy for the treatment of diabetic wounds.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Tang Yibo,Liang Chaohao,Liao Honghong,Yin Wenjie,He Fengbing,Liu Dong,Zhang Yu,Zhang Jian
Background Acute lung injury (ALI) is a life‑threatening respiratory disease that lacks precise diagnostic tools and specific therapeutic interventions, highlighting an urgent need for theranostic strategies. Here, we developed a biomimetic multienzyme‑mimetic Prussian blue nanozyme (MM@HMPB/Sim) that couples catalytic ROS neutralization with macrophage reprogramming for photoacoustic (PA) imaging‑guided immunotherapy of ALI. Results The nanoplatform was constructed by cloaking simvastatin (Sim)‑loaded hollow mesoporous Prussian blue (HMPB) metal–organic framework (MOF) nanozyme with a native macrophage membrane (MM). The HMPB core exhibited catalase (CAT)‑, peroxidase (POD)‑, and superoxide dismutase (SOD)‑like activities, enabling cascade catalytic scavenging of reactive oxygen species (ROS). MM@HMPB/Sim efficiently scavenged ROS, alleviated oxidative cellular damage, promoted M1-to-M2 macrophage repolarization, and inhibited monocyte adhesion to inflamed endothelium via competitive receptor engagement. Mechanistically, the HMPB core appeared to upregulate NRF2-dependent antioxidant responses, while simvastatin seemed to enhance AMPKα1-mediated metabolic reprogramming. Their combination was associated with synergistic restoration of the PPARα/AMPKα1/NRF2 axis and suppression of NF-κB p65, correlating with reduced Th17 differentiation and IL-17A production, which may have facilitated a shift toward an M2-like phenotype. Together with MM-mediated inhibition of immune cell infiltration, these effects were accompanied by improved pulmonary immune homeostasis and attenuated lung injury. The nanozyme also displayed favorable biocompatibility and gradual in vivo clearance. Conclusion This biomimetic multienzyme‑mimetic nanozyme offers a safe, PA imaging‑guided catalytic immunotherapy that integrates ROS neutralization with synergistic metabolic and antioxidant pathway modulation to resolve ALI, holding translational potential for ROS-driven inflammatory lung diseases. Graphical
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CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Xueying An,Hanjie Zhang,Xujing Zhang,Minyi Cai,Yining Zhou,Hantao Cai,Tao Shen,Sheng zhao,Zhihong Xu,Hui Wei,Qing Jiang
A lycopene-loaded CeO₂ nanozyme (Ly@Ce) is developed to combat chondrocyte senescence for osteoarthritis therapy • Ly@Ce efficiently scavenges mitochondrial ROS, restores mitochondrial dynamics, and elevates NAD + levels • Ly@Ce reverses H₂O₂-induced dysregulation of the p53-p21 signaling axis • Ly@Ce suppresses SASP expression and shifts ECM metabolism toward an anabolic program • The nanozyme integrates redox/NAD + reprogramming with senescence pathway inhibition, offering a disease-modifying strategy for OA Osteoarthritis (OA) is strongly associated with chondrocyte senescence, driven by oxidative stress, mitochondrial dysfunction, and the ensuing senescence-associated secretory phenotype (SASP). Herein, we report a lycopene-loaded ceria nanozyme (Ly@Ce) designed to simultaneously address these interconnected pathogenic cues. Ly@Ce markedly reduced intracellular and mitochondrial reactive oxygen species (ROS), mitigated excessive mitochondrial fragmentation, and restored mitochondrial membrane potential in senescent chondrocytes, indicating robust recovery of mitochondrial fitness. Notably, Ly@Ce also elevated intracellular nicotinamide adenine dinucleotide (NAD + ) levels, making it an active metabolic modulator rather than a passive ROS scavenger. Transcriptomic profiling revealed that Ly@Ce reversed H 2 O 2 -induced dysregulation of the p53-p21 signaling pathway, accompanied by suppression of SASP-related genes and a shift of extracellular matrix metabolism toward an anabolic program, thus delaying OA progression. Collectively, these findings establish Ly@Ce as a bioinspired, catalytic antioxidant nanoplatform that combines redox and NAD + reprogramming with p53-p21 inhibition, offering a disease-modifying strategy for senescence-associated OA and a potential framework for targeting other age-related pathologies characterized by mitochondrial decline and cellular senescence.
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Journal of Materials Chemistry B
·
2025
·
IF 5.7
Yu Guan,Jinyu Liu,Jing Yang,Sufang Chen,Weifeng Yao,Shengyuan Gong,Chunsheng Xiao,Mingqiang Li,Gangjian Luo,Ziqing Hei
Hepatic ischemia-reperfusion injury (IRI) is characterized by an acute surge of reactive oxygen species (ROS) upon reperfusion, leading to oxidative damage and cell death. Ferroptosis, a form of iron-dependent lipid peroxidation-driven cell death, has recently been implicated in hepatic IRI, compounding the injury. Here, we present an oxidation-responsive nanoparticle system designed to mitigate liver IRI by scavenging ROS and inhibiting ferroptosis. We synthesized a PEGylated poly(α-lipoic acid) (PEG-PαLA) copolymer that self-assembles into nanoparticles encapsulating the lipophilic antioxidant coenzyme Q10 (CoQ10). The PEG-PαLA/CoQ10 nanoparticles have an average diameter of ~100 nm and release CoQ10 preferentially under oxidative conditions. In vitro, the nanoparticles efficiently neutralized free radicals and protected hepatocytes from oxidative injury. In a mouse model of partial hepatic IRI, treatment with PEG-PαLA/CoQ10 nanoparticles significantly reduced liver injury markers, preserved liver histology, and abrogated lipid peroxidation, indicating suppression of ferroptosis. Our results demonstrated that PEG-PαLA/CoQ10 nanoparticle is a novel antioxidant nanomedicine that synergistically attenuates ROS-mediated damage and ferroptotic cell death in hepatic IRI. These findings highlight a promising strategy for protecting organs from ischemia-reperfusion damage by targeting oxidative stress and ferroptosis with responsive biomaterial carriers.
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Advanced Composites and Hybrid Materials
·
2026
·Vol. 9
·期 1
·91
·
IF 21.8
Fang Xuan,Zhao Hongqi,Ke Wentao,Zou Yi,Xu Tao,Chen Guangzi,Li Jian,Sheng Gaohong,Cheng Haozhe,Zhu Hao,Xiao Jun,Toh Wei Seong,Lin Sien,Wang Tianqi,Ma Tian
Osteoarthritis (OA) is a chronic joint disorder characterized by synovial inflammation, cartilage degradation and macrophage polarization imbalance, where excessive reactive oxygen species (ROS) accumulation and mitochondrial dysfunction exacerbate pro-inflammatory M1 macrophage polarization. Here, a pH-responsive nanocomposite (Se/LDH@PEG-M) is developed by integrating selenium (Se) within MgAl-layered double hydroxide (MgAl-LDH), modified with PEGylation and loaded with the mitochondria-targeted antioxidant Mito-TEMPO. The synthesized nanocomposite retains glutathione peroxidase (GPX)-like activity and the antioxidant capacity of Se nanoparticles, while exhibiting pH-responsive degradation to neutralize acidic OA microenvironments and release Mg²⁺, Se and Mito-TEMPO for inflammation suppression, ROS scavenging and macrophage polarization modulation. In vitro, Se/LDH@PEG-M effectively inhibits pro-inflammatory M1 polarization while promoting anti-inflammatory M2 phenotypes by suppressing multiple inflammatory pathways, restoring redox homeostasis, and enhancing mitochondrial oxidative phosphorylation and ATP production via respiratory chain activation. Conditioned medium from Se/LDH@PEG-M-treated macrophages attenuates chondrocyte apoptosis, inflammation and catabolism compared to LPS group. In murine OA models, intra-articular Se/LDH@PEG-M administration effectively alleviates synovial inflammation, suppresses osteophyte formation and mitigates cartilage degradation. This multifunctional nanocomposite concurrently targets OA pathogenesis through macrophage immunomodulation, ROS scavenging and mitochondrial protection, providing a potential therapeutic strategy for OA management. Graphical Schematic illustration of the synthesis process and therapeutic mechanism of Se/LDH@PEG-M. ( A )The synthesis procedure of Se/LDH@PEG-M nanocomposites. The nanocomposites were developed by integrating selenium (Se) into Mg-Al layered double hydroxides, followed by PEG modification and loading with mitochondria-targeted antioxidant Mito-TEMPO. ( B ) The therapeutic mechanism of Se/LDH@PEG-M. The nanocomposites degraded in acidic OA microenvironments and releasing Mg²⁺, Se and Mito-TEMPO for inflammation suppression, ROS scavenging and immunomodulation.
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RSC Advances
·
2026
·Vol. 16
·期 14
·12458-12474
·
IF 6.1
Xin Bao,Jingyan Sun,Xing Gao,Mingsheng Xu,Chen Dong,Honghua Pan
Spinal cord injury (SCI) is a severe type of central nervous system trauma. It not only causes the loss of sensory and motor function but also triggers a series of secondary injuries, especially oxidative stress and inflammation. Current therapeutic methods fail to effectively address the multi-pathological cascade reactions, highlighting an urgent need for integrated treatment strategies that can simultaneously repair the damaged microenvironment and promote neural regeneration. In this study, a multifunctional thermosensitive MNE@PDA-Diz/GP hydrogel was designed. We incorporated a core–shell structured manganese nanozyme@polydopamine (MNE@PDA), modified with dizocilpine, into gelatin methacryloyl and a poly(N-isopropylacrylamide) hydrogel (GP hydrogel), featuring a thermosensitive polymer. The MNE@PDA-Diz/GP hydrogel, which was crosslinked under UV-vis light, provides a biocompatible three-dimensional scaffold that mimics the natural mechanical properties of the spinal cord, thereby supporting cell adhesion and proliferation. Meanwhile, the photothermal properties of polydopamine and the thermosensitivity of poly(N-isopropylacrylamide) enable spatiotemporally controlled release of dizocilpine. These three components work in synergy: the manganese nanozyme scavenges reactive oxygen species to exert anti-oxidative effects, polydopamine modulates macrophage polarization to alleviate inflammation, and dizocilpine inhibits calcium influx to provide neuroprotection. This work presents a novel and versatile platform for multi-targeted SCI therapy and promotes the development of regenerative strategies.
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PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
·
2026
·
IF 4.8
Zibo Yin,Jusong Liu,Qianmei Pang,Yunfei Zhang,Lanying Wang,Yanping Luo
Cyromazine (CYR) is a widely used insect growth regulator. Its metabolite, melamine, is classified as a Group 2B carcinogen and has been associated with urinary tract lesions and tumors. While previous toxicological studies have largely focused on high-concentration exposures, the mechanisms of toxicity at environmentally relevant concentrations remain poorly understood. In this study, using Caenorhabditis elegans as a model, we demonstrated that CYR induces dose-dependent neurotoxicity, developmental impairment, reproductive toxicity, and oxidative stress. Transcriptomic analysis revealed disruptions in glutamate, dopamine, GABA, and glutathione metabolic pathways. CYR exposure caused damage to dopaminergic and glutamatergic neurons, decreased levels of several neurotransmitters, and downregulated key genes including dop-3 , tph-1 , and eat-4 , resulting in behavioral deficits such as impaired pharyngeal pumping, body bending, and head thrashing. Parental exposure to CYR significantly elevated reactive oxygen species (ROS) and lipofuscin accumulation, activated the glutathione-mediated antioxidant pathway, and disturbed enzymatic balance, indicating a central role for oxidative stress in CYR-induced neurotoxicity. By systematically elucidating the mechanism of ROS-mediated oxidative stress in neurobehavioral toxicity, this study provides a mechanistic foundation for understanding the broader toxicological profile of CYR, thereby offering critical insights for assessing its comprehensive health risks at environmental levels.
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Small
·
2023
·Vol. 19
·期 17
·2206936
·
IF 13.3
Jiahui Yan,Yanan Wang,Jingwen Zhang,Xiaohu Liu,Liangmin Yu,Zhiyu He
Calcium overload and ROS overproduction, two major triggers of acute kidney injury (AKI), are self-amplifying and mutually reinforcing, forming a complicated cascading feedback loop that induces kidney cell “suicide” and ultimately renal failure. There are currently no clinically effective drugs for the treatment of AKI, excluding adjuvant therapy. In this study, a porous silicon-based nanocarrier rich in disulfide bond skeleton (<50 nm) is developed that enables efficient co-loading of the hydrophilic drug borane amino complex and the hydrophobic drug BAPTA-AM, with its outer layer sealed by the renal tubule-targeting peptide PEG-LTH. Once targeted to the kidney injured site, the nanocarrier structure collapses in the high glutathione environment of the early stage of AKI, releasing the drugs. Under the action of the slightly acidic inflammatory environment and intracellular esterase, the released drugs produce hydrogen and BAPTA, which can rapidly eliminate the excess ROS and overloaded Ca 2+ , blocking endoplasmic reticulum/mitochondrial apoptosis pathway (ATF4-CHOP-Bax axis, Casp-12-Casp-3 axis, Cyt-C-Casp-3 axis) and inflammatory pathway (TNF-α-NF-κB axis) from the source, thus rescuing the renal cells in the “critical survival” state and further restoring the kidney function. Overall, this nanoparticle shows substantial clinical promise as a potential therapeutic strategy for I/R injury-related diseases.
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