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Advanced Healthcare Materials · 2026 · IF 11

A Pathological Microenvironment–Responsive Catalytic Carbon Nanodots Release Platform Intercepting the ROS–Inflammation Cascade to Alleviate Intervertebral Disc Degeneration

Xiang Luo,Jiajun Xie,Fengxu Yan,Zhidong Peng,Chongzhi Pan,Yiming Hu,Jian Zhang,Changxiong Cai,Jinghong Yuan,Yang Li,Xinxin Miao,Dingwen He,Xigao Cheng

Localized oxidative stress and chronic inflammation driven by excessive accumulation of reactive oxygen species (ROS) represent central pathogenic forces that initiate and perpetuate the degenerative cascade underlying intervertebral disc degeneration (IVDD). Here, it is developed a pathological microenvironment–responsive catalytic carbon nanodot delivery platform (PPOD@CeCDs) featuring dual reversible covalent cross-linking mediated by phenylboronate ester and Schiff base bonds, which selectively senses the acidic and highly oxidative milieu characteristic of IVDD to enable on-demand release of cerium-doped carbon nanodots (CeCDs), thereby intercepting the ROS-driven inflammatory cascade at its oxidative origin. PPOD@CeCDs exhibits favorable injectability, controllable degradability, biocompatibility, and robust antioxidant activity, together with stable intradiscal retention and stimulus-responsive release under pathological conditions. In vitro, PPOD@CeCDs protects nucleus pulposus (NP) cells from oxidative injury, suppresses inflammation amplification by modulating the ROS-driven PI3K–Akt–NF-κB signaling axis, regulates macrophage polarization, and preserves extracellular matrix homeostasis. In a rat model of IVDD, intradiscal injection of PPOD@CeCDs mitigates matrix degradation and promotes structural restoration of degenerative discs. Collectively, by integrating a microenvironment-responsive hydrogel with catalytically active carbon nanodots, this strategy sustainably intercepts ROS-driven inflammatory cascades and offers a mechanistically defined, translationally promising therapeutic approach for IVDD.

✓ 已验证 DOI PubMed 高影响因子
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Biomolecules · 2026 ·Vol. 16 ·期 3 ·387 · IF 5.6

Multi-Target Photoprotection by Taxifolin Against UVB-Induced Keratinocyte Injury Through UVB Filtration, ROS Scavenging and Transcriptomic-Proteomic Reprogramming

Fangfang Chen,Yihan Cai,Jinxiong Wu,Nengzhen Fang,Fei Li,Hongtan Wu,Yu-Pei Chen

Taxifolin, a natural flavonoid, consistently exerts cytoprotective effects against various oxidative stresses. In this study, we systematically evaluated its photoprotective efficacy and underlying mechanisms against ultraviolet B (UVB)-induced injury in human immortalized keratinocytes (HaCaT). Cell viability and apoptosis were assessed by MTT, fluorescence staining, and flow cytometry, while integrative transcriptomic and proteomic analyses were employed to identify core pathways and key mediators. Taxifolin exhibited antioxidant capacity comparable to that of ascorbic acid under identical in vitro radical-scavenging assays. Moreover, it displayed a strong absorption peak at 289 nm that overlaps the UVB spectrum (280–320 nm), enabling it to act as a chemical sunscreen. In UVB-challenged HaCaT cells, taxifolin markedly reduced intracellular reactive oxygen species (ROS) and attenuated JNK/p38 MAPK activation, as evidenced by Western blot, thereby breaking the ROS-MAPK vicious cycle. Multi-omics revealed that taxifolin was associated with attenuation of UVB-imposed G1/S arrest concomitant with restored Cyclin expression, while up-regulating MYC, FOXQ1, HMOX1 and AP-1 components c-Jun/c-Fos and thereby switching on a pro-survival transcriptional program. Consequently, apoptosis was suppressed and survival was significantly improved. Collectively, taxifolin integrated chemical filtration, ROS scavenging and signaling modulation to support a multi-target photoprotective network, which provides mechanistic insight into taxifolin-mediated cytoprotection and identifies candidate molecular nodes for further validation.

CAS / MDL: 480-18-2
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JOURNAL OF NANOBIOTECHNOLOGY · 2026 ·Vol. 24 ·期 1 ·491 · IF 15

A ROS-responsive core–shell microneedle platform integrating sonodynamic gas antibacterial therapy and modulating immunity for diabetic wound healing

Wang Pinkai,Ai Fanrong,Huang Guanfeng,Shen Yunfeng,Cui Fengyang,Deng Hui,Liang Chengzhi,Xie Jiajun,Kang Jiawei,Zhu Yudan,Xiong Weixiang,Tao Jun

Chronic diabetic wounds complicated by biofilm infections resist healing because persistent bacterial colonization coexists with microenvironmental imbalances, including oxidative stress and inflammation. Conventional pharmacotherapy and wound care are limited by impaired local perfusion, which hinders both effective biofilm eradication and reversal of the pathological wound microenvironment. We developed an ultrasound-activated core–shell microneedle platform (CCA&Lut@MN) that combines sonodynamic gas cascade antimicrobial therapy with a ROS-responsive microenvironment modulation strategy. Upon ultrasonic stimulation, L-arginine–modified copper–cysteine nanoparticles (CCA) in the microneedle shell generate reactive oxygen species (ROS) and catalyze NO release from L-Arg, producing synergistic oxidative and nitrative stress that yields rapid bactericidal activity and effective biofilm eradication. The microneedle core consists of an ROS-responsive PVA-HP-luteolin hydrogel that degrades in response to elevated ROS in the microenvironment, releasing luteolin. Luteolin scavenges excess ROS and promotes macrophage polarization to the M2 phenotype, thereby enhancing angiogenesis and cell migration. In a diabetic rat wound model infected with MRSA , CCA&Lut@MN markedly reduced wound bacterial load, alleviated local inflammation and improved blood supply, and thereby accelerated wound healing. This microneedle platform produces synergistic antibacterial effects via sonodynamic therapy (SDT)–gas cascade reactions, modulates the pathological microenvironment, and improves local blood supply, offering a promising strategy for treating complex and refractory wounds. Graphical The alternative text for this image may have been generated using AI.

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SEPARATION AND PURIFICATION TECHNOLOGY · 2026 · IF 9.1

Micronano bubble-enhanced microbial inactivation during water disinfection by underwater plasma discharges: surfactant-mediated ROS retention and subcellular mechanisms

Mengying Zhu,Shuai Yuan,Chenyu Liu,Xiaoran Wang,Zhuo Li,Yue Feng,Rusen Zhou,Anton Nikiforov,Dingxin Liu,Renwu Zhou

Microbial safety remains a critical global challenge for public health and the environment, exacerbated by escalating antimicrobial resistance and increasingly stringent regulations on disinfection by-products. Plasma-activated water (PAW) emerges as a promising antimicrobial medium, yet its efficacy is constrained by the rapid decay of key reactive species. Micro-nano bubbles (MNBs) may enhance species transfer and persistence, but the interfacial mechanisms governing bubble controllability and the resulting impacts on PAW lifetime remain insufficiently understood. Here, we investigate how surfactant-mediated interfacial modulation regulates bubble characteristics and reactive species retention within an in situ plasma-bubble system. Nonionic surfactants substantially increase bubble density, narrow the microbubble size distribution while reducing zeta potential. In contrast, the anionic surfactant sodium dodecyl sulfate (SDS) is found to exert minimal influence on zeta potential, but significantly enhances O 3 retention for at least 30 min. This modulation extends the bactericidal lifetime of PAW from less than 10 min to 100 min post-discharge. Scavenger assays and intracellular ROS measurements further identified superoxide (·O 2 − ) as a critical species sustaining the bioactivity of PAW. Mechanistically, SDS appears to maintain ·O 2 − level through two complementary pathways: (i) physically stabilizing ROS level by improving bubble properties and (ii) altering interfacial chemistry and associated radical interactions. Overall, these findings highlight the role of interfacial chemistry in plasma–liquid interactions and provide a practical strategy for achieving sustained antimicrobial performance of PAW.

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JOURNAL OF NANOBIOTECHNOLOGY · 2026 · IF 15

Black phosphorus nanosheet-enabled ROS-adaptive core-shell microneedles orchestrate immunoredox remodeling and neurotrophic regeneration for facial nerve repair

Zhou Qiang,Yuan Qingyue,Lai Peng,Li Shuo,Wang Xianlong,Han Yuqi,Lin Shuyi,Fang Chenhao,Qu Kaizheng,Zhang Ziwei,Ran Ying,Yang Yiheng,Ertas Yavuz Nuri,Liu Liangle,Chen Xianzhen

Background Facial nerve injury often results in persistent facial paralysis because the early oxidative and inflammatory microenvironment compromises subsequent neurotrophic repair. Existing therapies are limited by insufficient spatiotemporal control over antioxidative and neurotrophic interventions at the lesion site, leading to suboptimal regenerative outcomes. Black phosphorus nanosheets (BPNs) have emerged as promising nanotherapeutics owing to their strong ROS-scavenging capacity, immunomodulatory potential, and favorable biodegradability. However, strategies that integrate BPN-mediated microenvironment regulation with sustained neurotrophic stimulation for facial nerve repair remain largely unexplored. Here, we developed a ROS-adaptive core–shell microneedle nanoplatform that sequentially remodels the oxidative–inflammatory niche and subsequently promotes neurotrophic regeneration through staged delivery of BPNs and nerve growth factor (NGF). Results The microneedle shell consisted of a dynamic hyaluronic acid–phenylboronic acid/poly(vinyl alcohol) network loaded with BPNs, while the GelMA hydrogel core served as a reservoir for sustained NGF release. Under ROS conditions, cleavage of boronate ester bonds accelerated shell degradation and promoted BPN release. The released nanosheets reduced intracellular ROS, were associated with NRF2/HO-1 antioxidant pathway activation and NF-κB inflammatory signaling suppression in macrophages, and promoted polarization toward a pro-regenerative M2-like phenotype. This immunoredox modulation reduced oxidative stress and inflammatory mediator expression while establishing a more permissive microenvironment for neural repair. Subsequently, controlled NGF release from the core enhanced TrkA/AKT/ERK signaling, promoting neuronal differentiation, neurite extension, and axonal regeneration. The platform also improved Schwann cell proliferation, migration, and neurotrophic secretion, supporting remyelination and axonal guidance. In a mouse facial nerve crush model, treatment with BPN/NGF core-shell microneedles reduced oxidative damage and inflammatory infiltration, improved myelin sheath integrity and nerve ultrastructure, and accelerated early functional recovery compared with blank or single-cargo microneedle treatments. Conclusion This study presents a BPN-enabled ROS-responsive microneedle nanoplatform that addresses stage-specific barriers in facial nerve repair by sequentially regulating immunoredox responses and stimulating neurotrophic signaling. These findings highlight a promising nanobiotechnology strategy for peripheral nerve regeneration and may provide a broadly applicable framework for ROS-associated tissue injuries. Graphical The alternative text for this image may have been generated using AI.

✓ 已验证 DOI PubMed 高影响因子
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International Journal of Pharmaceutics-X · 2026 · IF 7.9

ROS-responsive tegafur-pheophorbide a conjugate-loaded microneedles for deep drug delivery and chemo-photodynamic therapy of superficial tumors

Anning Li,Yingjie Ma,Yunfeng Dai,Yibin Guo,Yanjun He,Sihan Chen,Xinjie Su,Chenxi Fang,Long Chen,Meitao Duan,Ming Chen,Jungang Ren,Li Wang,Chen Wang,Zhiqiang Zhang

Superficial tumors, including breast cancer, melanoma, and oral carcinoma, pose significant treatment challenges due to their anatomical location and the inherent limitations of conventional therapies, such as systemic toxicity and poor tumor specificity. Chemotherapy often leads to severe side effects, while photodynamic therapy (PDT) is hindered by the limited tissue penetration of both light and photosensitizers. To address these issues, we developed an innovative reactive oxygen species (ROS)-responsive drug delivery system based on a conjugate of tegafur (TF) and pheophorbide a (PPa) linked via a thioether bond. This prodrug (TF-TA-PPa) integrates chemotherapy and PDT into a single molecular entity, enabling synergistic anti-tumor effects. To enhance localized delivery and patient compliance, the conjugate was encapsulated into polymeric micelles and further incorporated into soluble microneedles (MNs) containing cell-penetrating peptides. The resulting TF-TA-PPa@PMN system enables painless transdermal administration, deep tumor penetration, and on-demand drug release triggered by near-infrared laser irradiation through ROS-mediated cleavage of the thioether linker. Comprehensive in vitro and in vivo evaluations demonstrated excellent biocompatibility, sustained drug release profiles, enhanced cellular uptake, and potent tumor suppression in a 4 T1 breast cancer model, achieving a remarkable tumor inhibition rate of 89.2% with minimal systemic toxicity. This integrated platform represents a promising strategy for the localized, combinatory treatment of superficial tumors with improved efficacy and reduced side effects.

✓ 已验证 DOI PubMed 高影响因子
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ACS Applied Materials & Interfaces · 2026 · IF 7.8

Dandelion-Derived Carbon Dots with pH-Responsive Charge and Dual ROS Regulation for Anti-Infection and Accelerated Wound Repair

Peili Li,Siyu Zhang,Haoran Xu,Xiangxiang Wu,Xiaoqing Yu,Wenxin Wang,Ran Ding,Da Zhang,Junhua Chen,Xiang Ke,Zirong Li

Bacterial infections associated with biofilm formation hinder wound healing via enhanced antibiotic resistance and impaired tissue repair. Herein, we fabricated dandelion herb-derived carbon dots (DH-CDs) through a green solvothermal-extraction method, developing a biocompatible antimicrobial agent with synergistic wound healing potential. Physicochemical characterization showed that DH-CDs are quasi-spherical (4.87 nm), partially graphitized nanoparticles with abundant surface functional groups and pH-responsive charge-switching capability. In vitro studies demonstrated that DH-CDs exhibit broad-spectrum antibacterial activity against S. aureus and E. coli, with minimum inhibitory concentrations (MICs) of 62.5 μg/mL at pH 7.4 and 31.25 μg/mL at pH 5.5. The antibacterial effect is mediated by a multimodal mechanism involving electrostatically driven bacterial membrane disruption, energy metabolism inhibition, intracellular reactive oxygen species (ROS) generation, and antioxidant enzyme inactivation. Moreover, DH-CDs achieve complete disruption of mature S. aureus biofilms at 300 μg/mL. Notably, DH-CDs possess excellent biocompatibility, with a 10% hemolysis concentration (HC10) exceeding 4000 μg/mL and over 95% viability of NIH 3T3 fibroblasts at 2000 μg/mL. A unique dual ROS-modulating capability was identified that DH-CDs generate excessive ROS to eradicate bacteria while scavenging deleterious ROS in mammalian cells, thereby preserving redox homeostasis. In vivo evaluations in a murine S. aureus-infected full-thickness wound model demonstrated that DH-CDs significantly accelerate wound closure by promoting re-epithelialization, granulation tissue maturation, collagen deposition, and hair follicle regeneration, outperforming a commercial wound healing spray. Collectively, DH-CDs integrate green synthesis, pH-responsive antibacterial/antibiofilm activity, dual ROS regulation, and biocompatibility, representing a promising translational candidate for bacteria-infected wounds and a paradigm for multifunctional biomass-derived nanomaterials.

✓ 已验证 DOI PubMed 高影响因子
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Surfaces and Interfaces · 2026 · IF 6

Self-sufficient Fe/Mn@CuO₂ nanozyme with cascade ROS amplification and GSH depletion for superior antibiofilm and bactericidal performance

Lihua Fan,Yuhan Niu,Yanru Zhang,Di Wu,Yongning Wu,Guoliang Li

The escalating challenge of bacterial resistance necessitates the development of novel antibacterial agents, positioning the synthesis of nanomaterials as a pivotal strategy for controlling pathogenic bacteria in the food sector. In this study, a novel H₂O₂ self-supplying nanocomposite was developed, comprising Fe/Mn nanoparticles functionalized with cuprous oxide (CuO₂), denoted as Fe/Mn@CuO₂. This composite exhibit tandem peroxidase (POD)-mimetic and glutathione (GSH)-depleting activities, enabling the on-demand generation of hydroxyl radicals via self-produced H₂O₂ and O₂ under acidic conditions (pH 5.5). The synergistic integration of H₂O₂ self-generation, POD-like catalysis, and GSH consumption significantly enhanced reactive oxygen species (ROS) production, leading to efficient eradication of E. coli (99.4%) and Staphylococcus aureus (99.1%) and remarkably antibiofilm efficacy. This multi-mechanistic action induced pronounced morphological alterations and severe membrane disruption in both bacterial strains. Furthermore, Fe/Mn@CuO₂ demonstrated the ability to denature DNA/RNA, disrupt energy metabolism, and achieve potent bacterial inactivation without detectable cytotoxic side effects. This work marked a substantial advancement in overcoming the drawbacks of conventional bactericidal strategy by combining self-sustaining H₂O₂ supply, POD-like activity, and GSH depletion, thereby presenting a highly promising antibacterial platform. Download: Download high-res image (304KB) Download: Download full-size image

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JOURNAL OF NANOBIOTECHNOLOGY · 2026 · IF 15

A novel pH-responsive nanoreactor for pyroptosis induction: multifaceted ROS amplification drives potent immunotherapy against triple-negative breast cancer

Wenjia Liu,Ying Wang,Xiangyu Hao,Yangxun Wang,Xiaofan Zhang,Jinchao Zhang,Kun Ge,Guoqiang Zhou

Triple-negative breast cancer (TNBC) is associated with rapid progression and poor sensitivity to monotherapies, necessitating combination strategies to enhance tumor immunogenicity, reprogram the tumor microenvironment (TME), and convert immunologically "cold" tumors into "hot" ones. In this study, we develop a pH-responsive, pyroptosis-inducing nanoreactor, ZnS/ZIF-90:Fe/Vk3 (ZZFV), designed to elicit potent antitumor immunity. Under acidic conditions, ZZFV rapidly degrades, releasing Zn 2+ , Fe 2+ , H 2 S, and Vk3. H 2 S promotes glucose uptake and consumption while downregulating cytochrome c oxidase subunit IV (COX IV) expression, whereas Zn 2+ suppresses lactate dehydrogenase (LDH) activity, collectively disrupting glucose metabolism and exacerbating intracellular acidification. Meanwhile, NAD(P)H quinone oxidoreductase 1 (NQO1), highly expressed in tumor cells, catalyzes the conversion of Vk3 to H 2 O 2 , which is subsequently converted to highly toxic •OH through Fe 2+ -mediated Fenton reactions. Additionally, Zn 2+ and H 2 S synergistically disrupt mitochondrial function, thereby amplifying reactive oxygen species (ROS) production. Excessive ROS triggers Caspase-1-dependent pyroptosis, leading to the liberation of damage-associated molecular patterns. These events promote dendritic cell (DC) maturation, robust T-cell activation, M1 macrophage polarization, and expansion of central memory T-cell populations, thereby conferring durable immune protection. Consequently, ZZFV demonstrates potent antitumor efficacy, effectively overcoming immune tolerance in TNBC and achieving robust, sustained antitumor immunity.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF NANOBIOTECHNOLOGY · 2026 ·Vol. 24 ·期 1 ·578 · IF 15

PDA@MnOx nanozyme-engineered mesenchymal stem cells for severe acute pancreatitis therapy via modulation of ROS-inflammation-microbiota homeostasis

Zhao Zinan,Mutailipu Muladili,Mei Tianxiao,Cui Ran,Wang Yongkun,Liu Fuguo,Dong Chunxiu,Jia Wenwen,Liu Zhongmin,Chen Bo,Le Wenjun,Hu Yihui

Severe acute pancreatitis (SAP) is a life-threatening inflammatory disorder with an approximate mortality rate of 40%. Current therapeutic approaches fail to address its complex pathological microenvironment, necessitating novel synergistic strategies. Although mesenchymal stem cells (MSCs) exhibit therapeutic potential, their efficacy is significantly compromised by SAP-associated oxidative stress, hyperinflammation, and gut dysbiosis. Herein, we engineered MSCs with antioxidant nanozyme PDA@MnO x , named PDA@MnO x -MSCs ( Abbr. E-MSCs), to establish a regulatory network for SAP therapy. The PDA@MnO x nanozymes not only scavenge reactive oxygen species (ROS) to protect MSCs from oxidative damage but also enable in vivo T 1 -weighted MRI tracking. E-MSCs demonstrated enhanced anti-inflammatory effects, evidenced by reduced levels of TNF-ɑ and IL-6, and restored gut microbiota homeostasis, characterized by increased Bacteroidetes abundance. This further alleviated pancreatic necrosis and systemic inflammation. Notably, the synergistic interaction among PDA@MnO x nanozymes, MSCs, and the pathological microenvironment restored ROS-inflammation-microbiota homeostasis, significantly improving SAP outcomes. This study provides a multifunctional strategy integrating therapeutic efficacy, in vivo tracking, and gut microbiota modulation for SAP treatment. Graphical

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MATERIALS TECHNOLOGY · 2025 · IF 3.7

A hybrid hydrogel for enhanced ocular surface interaction and ROS clearance in dry eye disease management during general anesthesia

Guangrui Li,Shenglong Zhang,Qingyao Zhong,Meiling Weng

Dry eye disease (DED) is a common chronic ocular disorder leading to corneal epithelial cell injury and death during general anesthesia. Recent studies have focused on reactive oxygen species (ROS) clearance, but existing strategies lack the ability to prolong drug retention time and addressing both corneal epithelial cell protection and ROS clearance synergistically. Hydrogels have emerged as a promising approach. However, the application of tannic acid (TA) and Ce4⁺ in hydrogels for DED treatment remains underexplored. This study proposes a smart hydrogel based on gelatin, TA and Ce4⁺, forming a cross-linked network with dynamic covalent bonds. The hydrogel exhibited >90% ROS clearance efficiency, ~95% human corneal epithelial cell viability after 24 h of co-culture, and ~90% intracellular ROS clearance under oxidative stress. These results indicate that the Gel10-TA@Ce hydrogel effectively prevents oxidative damage while maintaining excellent cytocompatibility, addressing the limitations of current dry eye disease treatments.

CAS / MDL: 3326-32-7
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JOURNAL OF COLLOID AND INTERFACE SCIENCE · 2025 · IF 9.7

Near-infrared and pH dual-responsive chitosan/epigallocatechin gallate/hollow CuS hydrogel reprograms ROS dynamics for infected wound healing

Pami Yang,Yuancheng Liu,Qin Zeng,Shuang Zhao,Yi Zhang,Junhong Yang,Ke Yin,Wuming Wu,Chunyan Deng

Bacterial-infected wounds pose a clinical challenge requiring innovative strategies integrating precise antibacterial action and microenvironment reprogramming. To address this, a multifunctional H-CuS NPs@epigallocatechin gallate (EGCG)/chitosan (CS)/3-formylphenylboronic acid (3-FPBA) hydrogel (H-CuS@EGCG HY) was engineered. This hydrogel exhibits injectability, self-healing, tissue adhesion, and pH-responsive behavior. During the initial phase of wound infection (weakly acidic microenvironment), this network undergoes controlled dissociation, enabling on-demand localized release of EGCG and Cu 1+/2+ . Under near-infrared (NIR) irradiation, the photothermal effect of H-CuS NPs promotes mild heating, which enhances EGCG/Cu 1+/2+ release and penetration. The released Cu 1+/2+ further catalyzes •OH generation from H 2 O 2 via Fenton reaction, synergizing with EGCG and photothermal therapy to improve antibacterial efficacy. Additionally, EGCG scavenges excess radicals, reducing oxidative stress and inflammation, while Cu 1+/2+ supports angiogenesis via VEGF regulation-collectively reprogramming the wound microenvironment. In vitro tests showed broad-spectrum antimicrobial activity with a 99 % eradication rate. In S. aureus -infected mouse models, compared to the control group, the H-CuS@EGCG HY + NIR group significantly reduced the levels of inflammatory cytokines (TNF-α), promoted the expression of CD31 and CD206, and effectively modulated the wound microenvironment, ultimately resulting in complete wound closure (100 %) by day 13, accompanied by full epidermal regeneration and minimal scarring. This study provides a promising strategy for the treatment of clinical wounds.

CAS / MDL: 25535-16-4 9012-76-4
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