COLLOIDS AND SURFACES B-BIOINTERFACES
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2026
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IF 5.9
Qian Tang,Wen-Li Luo,An-Ni Guo,Yuan Chen,Zhen-Hua Liu,Jing-Wei Shao
Nanozyme heterostructures with extended light absorption into the visible region. • Chlorogenic acid-loaded microneedles enable bidirectional ROS regulation. • Dynamic redox homeostasis promotes M2 polarization and angiogenesis. • The microneedle platform enables synergistic antibacterial and wound-healing therapy. Burn wounds infected with Staphylococcus aureus (S. aureus) are often characterized by excessive early inflammation, which leads to persistent oxidative stress, pain, and delayed healing. To overcome the limitations of conventional photosensitizers, which may induce reactive oxygen species (ROS) overload and subsequent tissue damage, we developed a ROS-responsive microneedle patch (TC@MN). This system consists of chlorogenic acid–based microneedles encapsulating a CuₓO–TiO 2-X (TC) nanozyme heterostructure designed for synergistic antibacterial and regenerative therapy. TC@MN exhibits intrinsic peroxidase-like (POD) and catalase-like activities (CAT). Under light irradiation, these catalytic processes participate in ROS regulation and promote Cu²⁺/Cu⁺ redox cycling, leading to the generation of bactericidal •OH and •O₂⁻ radicals while simultaneously producing O₂ to alleviate local hypoxia. In animal experiments, TC@MN scavenges excess ROS and promotes macrophage polarization toward the M2 phenotype thereby facilitating inflammation resolution and tissue repair under light-free conditions. Collectively, this light/dark dual-mode microneedle platform integrates photocatalytic and enzyme-mimetic functions, offering a biocompatible and intelligent strategy for the treatment of infected burn wounds.
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Journal of Environmental Chemical Engineering
·
2026
·Vol. 14
·期 3
·122557
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IF 7.5
Xiaomeng Li,Yaning Ma,Ruimeng Li,Yan Ge,Jiapeng Tang
The integration of multifunctional protective materials capable of simultaneous defense against ultraviolet (UV) radiation, O 3 , and reactive oxygen species (ROS) remains a challenge in interfacial materials science, primarily due to difficulties in constructing stable and catalytically efficient interfaces on flexible substrates. Herein, we report a cellulose-guided interfacial engineering strategy for the in-situ growth of copper-based metal-organic framework (Cu-MOF) nanozymes on nylon/spandex fabric. The key to this strategy lies in the pre-coordination of Cu 2 + with the hydroxyl groups of cellulose, which molecularly guides the ordered crystallization of Cu-MOFs within a regenerated cellulose network at the fiber interface, yielding a nanosheet structure with enhanced density and accessibility of catalytic sites. The resulting cellulose-MOF hybrid is firmly anchored to the fabric through a synergistic dual mechanism: physical entrapment within the regenerated porous cellulose network provides structural integrity, while chemical coordination between Cu 2+ and cellulose hydroxyls directs oriented growth and reinforces interfacial adhesion. This precisely engineered interface enables exceptional cascade antioxidant activity (mimicking superoxide dismutase and catalase), high UV protection (UPF > 100), and rapid ozone decomposition (first-order kinetic constant k > 0.478 min −1 ). The material also demonstrates robust interfacial adhesion, ensuring mechanical durability, breathability, and wash durability (>30 cycles). Biocompatibility was confirmed by skin irritation tests. This work highlights the critical role of biomass-templated interfacial microstructure in regulating catalytic performance and provides a green, scalable paradigm for designing advanced functional interfaces for environmental and biomedical protection.
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POULTRY SCIENCE
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2026
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IF 4.5
Tian-Chi Tang,Rui-Li Zhang,Xiao-Yi Yang,Ling-Huan Luo,Xiang-Jie Wang,Kunpeng Niu,Ming Ge
2-Ethylhexyl diphenyl phosphate ( EHDPHP ) is a widely used novel organophosphorus flame retardant. In recent years, EHDPHP has been absorbed into humans and animals through contaminated environments and food intake, causing substantial adverse effects. Therefore, the biological toxicity of EHDPHP has aroused widespread interest among researchers. However, research on the toxic damage mechanism of EHDPHP on the kidneys of poultry is still relatively limited. This study predicted the target sites of EHDPHP through network toxicology and molecular docking. Subsequently, chickens were administered varying concentrations of EHDPHP by oral gavage, and kidney tissues were collected on days 14, 28 and 42 to elucidate its potential nephrotoxic mechanism. Network biology analysis indicates that the predicted targets of EHDPHP and its critical metabolite 5-OH-EHDPHP are significantly enriched in MAPK and apoptotic pathways. The results of molecular docking showed that both EHDPHP and 5-OH-EHDPHP had good binding ability with JNK1/2, suggesting that JNK1/2 was a potential target for EHDPHP. Experimentally, EHDPHP exposure was found to induce oxidative stress, mitochondrial damage and apoptosis in chicken kidneys. These results suggest that kidney injury may be mediated through the activation of the ROS/JNK signaling pathway and the subsequent triggering of apoptosis. In conclusion, our study offers a foundation for further toxicological evaluation and mechanistic investigation of contaminant EHDPHP.
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Immunity & Ageing
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2026
·Vol. 23
·期 1
·12
·
IF 8.3
Sun Ruiqing,Luo Lan,Chen Yang,Sun Liangjie,Huo Yuhao,Ding Chong,Wang Yixiang
Background Senile osteoporosis (SOP) is becoming a critical public health burden particularly in aging societies due to escalating fracture susceptibility among elderly populations. Despite advances in SOP research, the mechanistic role of immune cell alterations in senile osteoporosis remains unclear. Methods As a validated SOP model, senescence-accelerated mouse prone 6 (SAMP6) mice were used for mechanistic studies, comparing with age- and gender-matched controls-senescence-accelerated mouse resistant 1 (SAMR1) mice. We combined micro-CT, molecular biology and histological techniques to assess the bone mineral density in femurs. To investigate dynamic interactions and differential pathways of immune cells within the bone marrow microenvironment, we employed a multi-omics integration strategy including single-cell RNA sequencing, transcriptome sequencing and flow cytometry. Furthermore, we conducted multicolor immunofluorescence and multiplex cytokine analysis to verify the above results. Moreover, we utilized BaF3 and RAW 264.7 cell lines to study the cell interactions during osteoclastogenesis and BX471(a CCR1 antagonist) was used to block this process. Results SAMP6 mice showed a marked decline in bone mass accompanied by elevated reactive oxygen species (ROS) level in 3-month-old. The single-cell RNA sequencing of bone marrow revealed that a prominent depletion of B lymphocytes, with pro-B cells exhibiting the most pronounced reduction. Multi-omics integration analysis of pro-B cells suggested a significant activation of the Fos/Jun (AP-1) transcription complex accompanied by upregulation of chemokine CCL3 in the SAMP6 group. In vitro assays showed that H 2 O 2 -induced oxidative stress in BaF3 cells triggers Fos/Ccl3 axis activation and promoted osteoclastogenesis in RAW 264.7 cells. Moreover, blocking CCR1 with BX471 could suppress this effect. Conclusions Our findings suggest that the elevation of ROS levels within bone marrow microenvironment accelerates immune-senescence of B lymphocytes, characterized by a significant reduction in progenitor B-cell populations, which subsequently activates the Fos/Jun-mediated stress signaling pathway. The cascade ultimately results in the overexpression of CCL3, further promoting osteoclastogenesis of macrophage through CCL3-CCR1 axis. CCR1 antagonist could alleviate pro-inflammatory osteoclast formation, revealing a potential therapeutic target for senile osteoporosis.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2026
·Vol. 74
·期 30
·23947-23964
·
IF 6.7
Zhou Xinyue,Yu Wenxin,Cui Yanhong,Meng Xiang,Zhang Jian,Jiang Qingxue,Yang Bo,Ma Xiaoran,Ma Lin,Liang Qingwei,Wang Xuemin
Salt stress disrupts photosynthesis, ion homeostasis,
and antioxidant
systems, thereby inhibiting plant growth and reducing the yield and
quality. This study investigated the physiological and molecular mechanisms
of salt stress alleviation by foliar application of different concentrations
of silicon dioxide nanoparticles (SiO 2 NPs) in oats under
150 mM NaCl. Physiological and transcriptomic analyses were performed.
300 ppm of SiO 2 NPs significantly promoted growth and photosynthesis,
enhanced antioxidant enzyme activities, reduced oxidative damage,
and maintained Na + /K + balance while improving
nutritional quality. SiO 2 NPs regulated genes involved
in photosynthesis and carbon metabolism and upregulated the ion transporter
genes HKT1;1 , HKT7 , and HKT9 and ROS signaling genes MPK6 and WRKY33 . HKT proteins were localized to the plasma membrane.
Weighted correlation network analysis (WGCNA) identified six hub genes
associated with the growth and photosynthetic traits. Overall, SiO 2 NPs enhance salt tolerance, yield, and quality in oat by
maintaining Na + /K + homeostasis, activating ROS
signaling, and sustaining photosynthesis and carbon metabolism.
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BIOMATERIALS
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2026
·
IF 13.6
Canyi Chen,Qinqing Tang,Qinyao Xu,Dehui Feng,Qiang Luo,Bin Xu,Hanyuan Zhang,Tingting Zhao,Weijun Fang
Targeted autophagy regulation holds great promise for antitumor therapy, whereas conventional single-modal autophagy interventions easily induce compensatory escape of tumor cells and fail to transform protective autophagy into a lethal phenotype. In this study, a near-infrared (NIR)-responsive polypyrrole/zeolitic imidazolate framework-8 (PPy/ZIF-8) nanoparticle was successfully fabricated. This nanoplatform enables synergistic and precise regulation of autophagic flux, which amplifies upstream autophagy activation and blocks downstream autophagic pathways simultaneously. The incorporation of PPy endows the nanoparticle with excellent near-infrared absorption capability and photothermal effects. It boosts interfacial electron transfer and optimizes electron-hole separation, further enabling the nanoparticles to possess ROS generation ability. Under 808 nm laser irradiation, the generated ROS and zinc ions induce mitochondrial damage to amplify upstream autophagic signals, whereas the photothermal effect impairs lysosomal function and blocks the downstream degradation of autophagosomes. This dual regulatory strategy causes pathological accumulation of autophagosomes and ultimately triggers autophagic cell death in tumor cells. This work validates the feasibility of integrated autophagy regulation and provides a facile and versatile strategy for the design of advanced multimodal antitumor nanotherapeutics.
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BMC BIOTECHNOLOGY
·
2026
·
IF 4.8
Guan Junjie,Chen Xiaoqing,Cheng Jiaqi,Lu Yang,Chen Xiangdong
Severe inflammatory reactions and increased levels of reactive oxygen species (ROS) significantly worsen the degenerative progression of spinal cord injury (SCI). Extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) can alleviate inflammation associated with SCI, although their yield is limited. Conversely, MSC-extruded nanovesicles (NVs) possess therapeutic potential and exhibit significantly higher levels than EVs. In this study, an ROS-nanoscaffold (RNS + NVs) was developed for the treatment of SCI. NVs were produced from MSCs via physical extrusion and incorporated into an ROS-nanoscaffold (RNS). RNS + NVs effectively scavenged and degraded ROS, enabling the responsive release of NVs. NVs inhibited pro-inflammatory changes and decreased IL-6 and TNF-α release from lipopolysaccharide-induced BV2 cells, demonstrating anti-inflammatory activity similar to that of EVs. Furthermore, NVs exhibited a more pronounced antioxidative effect than EVs and successfully mitigated oxidative stress-induced damage in H 2 O 2 -induced PC12 cells. Moreover, in SCI models, NV absorption is predominantly mediated by the microglia and neurons. RNS + NVs have shown synergistic benefits in modulating the adverse in vivo microenvironment during the acute stage, consequently creating a favorable setting for tissue healing, long-term locomotion, and alleviation of neuropathic pain. RNS + NVs demonstrated significant potential as antioxidant and anti-inflammatory agents in SCI.
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ANTIOXIDANTS & REDOX SIGNALING
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2026
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IF 6.8
Jiaxue Tian,Huimin Wang,Huimin Liu,Wenlu Xu,Mengting Xiao,Xuemei Qin,Xiaojie Liu
Aims:Depression is a prevalent mood disorder with significant suffering and heightened suicide risk. Accumulating evidence points to oxidative stress and impaired energy metabolism of the brain as key contributors to the pathogenesis of depression. Astragaloside IV (AIV) has been demonstrated to alleviate neurological damage. The capacity of AIV for antioxidation has also been gradually discovered. Yet, it still just scratches the surface of the antidepression mechanisms of AIV. Our aim was to explore a novel mechanism of action of AIV from the perspectives of redox homeostasis and energy metabolism via the reactive oxygen species (ROS)/nuclear factor erythroid 2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1) axis.Results:AIV ameliorated anxiety and cognitive dysfunction in rats with depression-like behaviors. Furthermore, we illustrated that AIV reversed redox dyshomeostasis of rats with depression-like behaviors in terms of decreasing the level of malondialdehyde while increasing the abundances of catalase, superoxide dismutase, and glutathione peroxidase. In addition, AIV significantly increased the levels of indicators of energy metabolism that were interrupted by depression. Furthermore, in vitro, AIV significantly increased the levels of indicators related to the Nrf2/Keap1 signaling pathway in corticosterone-induced PC12 cells.Innovation:For the first time, it demonstrates that AIV alleviates depression by modulating the ROS/Nrf2/Keap1 axis and restoring hippocampal energy metabolism in a chronic unpredictable mild stress model.Conclusion:The current findings not only offer novel insights into antidepressant-like effects of AIV through the ROS/Nrf2/Keap1 axis but also provide a foundation for enhancing clinical efficiency and enriching drug selection. Antioxid. Redox Signal. 00, 000–000.
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS
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2026
·
IF 5.4
Lei Nie,Yingying Liang,Li Li,Guangrong Zheng,Ling Wang,Guanghai Fei,Wei Guo
Designing multifunctional hydrogel bio-adhesives that simultaneously scavenge reactive oxygen species (ROS) and regulate macrophage polarization to achieve injury sealing and tissue regeneration efficiently remains challenging. In this work, we developed a potent hydrogel bio-adhesive by borate crosslinking of phenylboronic acid conjugated hyaluronic acid (HA-PBA) and dopamine conjugated chondroitin sulfate (CHS-DA). The influence of varying HA-PBA/CHS-DA ratios on hydrogel properties was systematically investigated. The hydrogels were characterized using techniques including Fourier transform infrared spectroscopy, nuclear magnetic resonance spectroscopy, scanning electron microscopy, and reactive oxygen species scavenging assays. Results showed that the hydrogels exhibited good injectability and strong adhesion to the surfaces of various materials and organs, including rubber, metal, plastic, skin, heart, liver, stomach, and tongue. In addition, the bio-adhesives also displayed excellent cytocompatibility, cell pro-migration ability, pro-angiogenic capacity, and efficient intracellular reactive oxygen species scavenging. Furthermore, the hydrogel bio-adhesives demonstrated efficient intracellular ROS scavenging in fibroblast and RAW 264.7 cells. Moreover, the bio-adhesives revealed efficient macrophage polarization potential, shifting from pro-inflammatory (M1) to anti-inflammatory (M2). The available results confirmed the potential of the developed hydrogel bio-adhesives for injury-healing and tissue-regeneration applications.
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ACS Applied Polymer Materials
·
2026
·
IF 5.2
Pian Hou,Yue Zhang,Yinchao Cheng,Shuiping Ouyang,Caoxing Huang,Xin Zhou,Jing Luo,Liang Liu,Kankan Jiang
To overcome the dual challenges of excessive reactive oxygen species (ROS) and insufficient tissue adhesion in skin wound healing, this study developed a multifunctional hydrogel, designated Gam/Ct-HA@Czo, which integrates ROS-scavenging and tissue-adhesive capabilities. The hydrogel utilized methacrylated gelatin (Gam) as the polymeric matrix and incorporated chitin (Ct), hyaluronic acid (HA), and cerium–zirconium oxide (Czo) nanoparticles to establish a multifunctional hydrogel system. The developed hydrogel demonstrated an ROS scavenging efficiency of 46.8% and a tissue adhesion strength of 16.3 Kpa. It also possessed favorable antioxidant properties, self-healing capacity, and in vitro biocompatibility, which supported its role in effectively promoting tissue regeneration and repair. In a mouse full-thickness skin defect model, treatment with Gam/Ct-HA@Czo hydrogel significantly accelerated wound closure, promoted epithelial regeneration, and facilitated the orderly deposition of collagen. The findings demonstrate that the rational integration of multifunctional components into a hydrogel system offers a promising strategy for enhancing wound repair and regeneration.
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SEPARATION AND PURIFICATION TECHNOLOGY
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2026
·
IF 9.1
Jing Li,Jinquan Wan,Yan Wang
In peroxymonosulfate (PMS)-based advanced oxidation processes (AOPs), the precise regulation of reactive oxygen species (ROS) generation pathways is a core challenge for achieving selective degradation of target pollutants. In this study, we propose an electronic effect-guided ligand functionalization strategy by systematically introducing electron-donating (-OH, -NH 2 ) and electron-withdrawing (-NO 2 ) groups into the MIL-101 (Fe) framework, thereby establishing a quantitative structure-activity relationship between the electronic structure, coordination environment of Fe centers and ROS generation. The results demonstrate that electron-donating groups (-OH, -NH 2 ) significantly promote the non-radical pathway dominated by singlet oxygen ( 1 O 2 ), achieving efficient degradation of the electron-rich pollutant sulfamethoxazole (SMX) with removal efficiencies of 93.0% and 91.2%, respectively. Notably, the 1 O 2 contribution rate in the MIL-101(Fe)-OH system reached 95.07%. Correlation analysis reveals a significant positive correlation between C O content and 1 O 2 contribution. Combined experimental characterization and DFT calculations indicate that the selective generation of ROS results from the synergistic effects of multiple factors, including electronic structure, adsorption energy, and charge transfer. Electron-donating groups enhance the electron density at the Fe center, elongate the Fe O bond length, and optimize PMS adsorption energy, thereby promoting the self-disproportionation of the key SO 5 •- intermediate to generate 1 O 2 . This work highlights the promotional role of functional group electronic effects on the non-radical pathway, elucidates the core mechanism governing ROS generation, and provides a mechanistic framework for the design of highly selective Fenton-like catalysts. Environmental implication This study employs an electron-effect-guided ligand functionalization strategy to systematically reveal the structure–activity relationship between the electronic structure and coordination environment of metal nodes in Fe-MOFs and the ROS generation. The electronic effects of functional groups enable the precise regulation of ROS, and electron-donating groups significantly promote nonradical pathways, thereby achieving efficient degradation of the electron-rich contaminant sulfamethoxazole. This work highlights the promotion of nonradical pathways by the electronic effects of functional groups, clarifies the core mechanism governing ROS generation, and provides new insights for the design of highly efficient and selective catalysts.
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JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2026
·
IF 5.2
Yuting Dong,Xiaodan Wang,Shize Wang,Kang Yang,Tong Xu,Hongjin Lin
DEHP induces thymus injury in chickens by activating the NF-κB/TNF-α pathway, triggering oxidative stress and PANoptosis. • QUE can alleviate the activation of the NF-κB/TNF-α pathway, oxidative stress and PANoptosis induced by DEHP in chickens. • QUE exerts a targeted effect on NF-κB, thereby mitigating DEHP-induced thymus injury in chickens. Quercetin (Que), a natural dietary flavonoid, possesses significant antioxidative and immunoregulatory properties. Di(2-ethylhexyl) phthalate (DEHP), a pervasive environmental endocrine-disrupting chemical, triggers oxidative stress (OS) and elicits immunotoxic effects in various species. However, whether Que can target NF-κB to alleviate DEHP-induced OS and PANoptosis in the chicken thymus remains unclear to date. To investigate the mechanism of thymus damage induced by DEHP and the intervention effect of Que, we established an in vivo chicken model treated with DEHP and/or Que. Based on the results of network pharmacology, molecular docking, molecular dynamics simulations, and Cell Thermal Shift Assay (CETSA), we predicted that NF-κB is the key target for the protective effect of Que. Subsequently, through H&E staining, CCK-8, immunofluorescence, Western blot and other techniques, we verified the effects of DEHP and/or Que on OS, the assembly of PANoptosome, and cellular PANoptosis in chicken thymus tissue and chicken lymphocyte cell line (MSB-1). Meanwhile, to clarify the key role of NF-κB in the above regulatory process, we conducted reverse validation experiments by introducing the NF-κB activator Act1 in cellular experiments. The results demonstrated that DEHP exposure markedly induces the upregulation of NF-κB and TNF-α(P<0.05), leading to a pronounced burst of reactive oxygen species (ROS) and consequent OS within the chicken thymus. This process further activates the ZBP1-mediated PANoptosis pathway, ultimately causing damage to chicken thymus tissue. Que intervention effectively suppresses NF-κB activation, blocking the transmission of the NF-κB/TNF-α/ROS signaling axis, thereby reversing DEHP-induced ZBP1-mediated PANoptosis in chicken thymus. Download: Download high-res image (290KB) Download: Download full-size image
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