Search Results (5,415)

The sorghum aphid (Melanaphis sorghi), a phloem-feeding insect pest, causes severe economic losses in sorghum-producing regions worldwide. During feeding, aphids secrete salivary proteins with potential effector functions that play pivotal roles in plant–insect interactions. However, relatively few secreted proteins and effectors have been characterized in M. sorghi. In this study, proteomic analysis of aphid-infested sorghum leaves identified 69 putative aphid-derived proteins. Bioinformatic analyses were subsequently used to predict signal peptides within these proteins. Among the five candidates with signal peptides, MsSP1 was further confirmed to be delivered into sorghum tissues during aphid feeding by immunoblotting using a specific anti-MsSP1 antibody. Functional characterization revealed that silencing the MsSP1 gene in aphids by RNAi interference significantly reduced aphid fitness on sorghum. Moreover, transient expression of MsSP1 in Nicotiana benthamiana suppressed cryptogein-induced cell death and hydrogen peroxide accumulation, indicating that MsSP1 interferes with plant immune responses. Collectively, these results suggest that MsSP1 may act as a virulence effector that enhances aphid performance while suppressing host defense. This study expands current knowledge of plant–aphid interactions and provides new insights that may facilitate the development of sustainable pest-management strategies. Full article

Frailty and osteoarthritis (OA) frequently coexist in older adults, yet the extent to which they share molecular programs across tissues remains unclear. We integrated bulk transcriptomics, peripheral immune and OA meniscal single-cell atlases, inferred cell–cell communication, and an in vitro myeloid–chondrocyte conditioned-medium model. Frailty-associated vastus lateralis and OA synovium shared a 16-gene program enriched for inflammatory and migratory processes, which was refined by protein–protein interaction analysis into a 15-gene hub module (Hub-15). Donor-aware pseudobulk analysis showed coordinated Hub-15 upregulation in CD8 T, natural killer, B, and monocyte/macrophage-like cells, with the highest scores in monocyte/macrophage populations. In the meniscal atlas, donor-level analysis of 7 normal and 6 OA donors identified a 20.5 percentage point lower proportion of inflammatory/stress cells and a 17.3 percentage point higher proportion of fibrochondrocyte-like cells in OA (both false discovery rate = 0.010), whereas state-specific Hub-15 differences were not significant after correction. Exploratory communication analysis nominated directionally consistent candidate myeloid-to-structural signaling axes, although none remained significant after multiple-testing correction. Conditioned medium from cytokine-primed THP-1 cells elicited inflammatory and matrix-catabolic responses in C28/I2 cells. These findings identify a cross-tissue, leukocyte-shared, and myeloid-enriched inflammatory program that converges across independent frailty and OA cohorts, providing a hypothesis-generating framework for future mechanistic testing. Full article

Background/Objectives: The interaction between malignant cells and the extracellular matrix (ECM) is a critical driver of tumor invasion. ECM remodeling and desmoplasia characterize the tumor microenvironment, facilitating both stromal fibrosis and malignant progression. This study was conducted to evaluate plasma cell infiltration across distinct stromal patterns in oral squamous cell carcinoma (OSCC) and investigate its association with stromal desmoplasia and immune evasion. Methods: A total of eighty-seven cases that were histopathologically diagnosed as OSCC were included in the study. Immunohistochemical staining for IgG4, CD138, VEGF, TGF-β 1, and CD31 was performed on deparaffinized tissue sections, and the plasma cell count was determined. Results: Distinct stromal architectural patterns were observed across different grades of OSCC. Stromal desmoplasia initiated with inflammatory cell infiltration into the stroma at an early stage, followed by infiltration of the dense collagenous stroma; both revealed dense plasma cell infiltrates. However, the difference in plasma cell density between OSCC grades was not shown to be statistically significant using the chi-square test and ANOVA (p = 0.761 and p = 0.152, respectively). Conclusions: Stromal desmoplasia and immune evasion are associated with dense plasma cell infiltration, suggesting that these cells may serve as a potential prognostic indicator of the invasive progression in OSCC. Full article

Aortic dissection (AD) is a severe vascular condition marked by abrupt onset, rapid progression, and heightened mortality rates. Vascular smooth muscle cells (VSMCs), the predominant cellular component of the arterial media, are essential for maintaining the structural integrity and functionality of blood vessels. Recent studies have associated Cysteine-rich protein 2 (CSRP2) with the advancement of several vascular diseases. The involvement of CSRP2 in AD progression is unclear. Aortic tissues were collected from patients for RNA sequencing and histological analysis. A mouse model of AD was created using β-aminopropionitrile monofumarate (BAPN), while VSMC phenotypic switching was induced by platelet-derived growth factor BB (PDGF-BB). Adeno-associated virus vector was used to overexpress CSRP2 in aorta. A variety of histopathological assays and biochemical analyses were applied to determine gene and protein expression patterns as well as uncover underlying molecular mechanisms. CSRP2 was significantly downregulated in both human and murine AD, and CSRP2 gene overexpression dramatically reduced BAPN-induced AD incidence and prevented animal mortality. CSRP2 could preserve a contractile VSMC phenotype, even though under PDGF-BB stimulation. Mechanistically, our findings reveal that CSRP2 directly interacts with p130 Crk-associated substrate (p130Cas; also known as BCAR1) and reduces its phosphorylation, which in turn inhibits the activation of extracellular signal-regulated kinase (ERK) signaling pathways, thereby preventing VSMC phenotypic switching induced by PDGF-BB. Our findings identify CSRP2 as a novel regulator of VSMC phenotypic modulation and a significant modulator of AD development, suggesting its potential as a target for early intervention for AD. Full article

Post-myocardial infarction (MI) remodeling is accompanied by metabolic stress, but the myocardial genes associated with copper handling are poorly defined. We sought to prioritize a tissue-derived candidate rather than establish a copper-dependent mechanism. Regional MI transcriptomes and an in-house left anterior descending coronary artery ligation mouse RNA-sequencing cohort were integrated with protein quantitative trait locus-based Mendelian randomization (MR). Follow-up comprised local and external tissue validation, cardiac single-cell RNA sequencing, Genotype-Tissue Expression co-expression, computational perturbation, and CRIP2 knockdown or overexpression in H9c2 cells exposed to hypoxia/reoxygenation (H/R). CRIP2 showed a nominal protective-direction MR association (odds ratio 0.831, 95% confidence interval 0.735–0.939; p = 0.0031), but did not pass the Bonferroni threshold. Crip2 was lower in the local MI model (p = 0.0168; n = 5 per group) and in an independent dataset. A prespecified lipoylated-tricarboxylic-acid module was negatively enriched after MI (normalized enrichment score −1.63; false discovery rate 0.012), whereas the broader copper-homeostasis set was not significant. Single-cell data localized Crip2 mainly to cardiomyocytes, but were not adequately replicated for condition-level inference. Under H/R, Atp7a was the only copper-handling transcript whose knockdown-by-oxygen interaction remained significant after adjustment (q = 0.0405). CRIP2 overexpression was associated with higher Cell Counting Kit-8 metabolic activity during H/R (interaction p = 0.00551), whereas the knockdown interaction was not significant. Copper abundance, mitochondrial function, and cuproptosis markers were not measured. The data prioritize CRIP2 for mechanistic study, but do not show that it regulates copper flux or post-MI remodeling. Full article

The world is facing a triple global crisis: climate change, loss of biodiversity, and pollution. Plastics, man-made polymers from primary fossil fuel sources, have pervasively entered almost every sector and thereby caused huge environmental pollution. Microplastic (MPs) sizes range between 1 μm and 5 μm, and nanoplastics are less than 1 μm in size, respectively. Behaviour, accumulation and movement of plastics in soil, water and air depend on their size. Smaller sizes of microplastics and nannoplastics can easily enter cells, tissues, and finally, the food chain, and pose growing ecological and health concerns due to their persistence. It also acts as an adsorbent and has the ability to penetrate food webs. Their diverse shapes, especially fibres, increase their dispersal and bioavailability in aquatic ecosystems. Recent findings indicate that microalgae contribute to the mitigation of microplastic pollution. Microalgae, diverse photosynthetic microorganisms ranging from 0.5 to 200 μm, interact with microplastics through processes such as adsorption, aggregation, and potential biodegradation mechanisms, including toxin systems or enzymes produced by the microalgae, utilising plastic polymers as carbon sources. The filamentous morphology of some species, such as Spirulina sp., increases the entrapment and potential degradation of microplastic fibres. It is essential to understand these interactions to construct sustainable means of mitigating microplastic pollution and recovering the aquatic ecosystem health. Microalgae produce enzymes such as lipases, esterases, and cellulases, which facilitate the biodegradation of plastics. Microalgae form biofilm on the surface of microplastics. They also secrete sticky extracellular polymeric substances (EPS) that cause the microplastic to sink to the bottom of the water body, which helps to remove microplastics from surfaces. This review summarises knowledge on microalgae–microplastic interactions, with a focus on their potential for bioremediation of microplastics and also sustainable conservation of the environment. Full article

Serotonin (5-hydroxytryptamine, 5-HT) is traditionally considered a neurotransmitter, but most of the body’s serotonin is peripheral and participates in vascular, hemostatic, inflammatory, and immune processes. This review summarizes current evidence on the role of peripheral serotonin in innate and adaptive immunity and evaluates its clinical relevance in inflammatory and immune-mediated diseases. The article synthesizes experimental and clinical data on serotonin sources, 5-HT receptors, SERT, serotonylation, and 5-HT-dependent regulation of neutrophils, monocytes/macrophages, mast cells, dendritic cells, T cells, and B cells. The reviewed data indicate that serotonin modulates leukocyte recruitment, platelet–immune interactions, NETosis, macrophage polarization, dendritic cell–T-cell communication, lymphocyte activation, vascular permeability, and tissue remodeling. Clinically, serotonergic mechanisms are implicated in sepsis, inflammatory bowel disease, autoimmune disorders, cardiovascular inflammation, thromboinflammation, and the tumor microenvironment. However, the direction of 5-HT effects is not uniform and depends on receptor subtype, cell type, local mediator concentration, disease stage, and tissue context. Serotonin should therefore be regarded as a context-dependent immunoregulatory mediator rather than an exclusively pro- or anti-inflammatory factor. Further studies are needed to standardize clinical measurements of serotonin and its metabolites and to define therapeutically relevant serotonergic targets. Full article

Non-healing wounds remain a clinical challenge due to their complex pathophysiology and limited therapeutic options. These conditions are driven by complex molecular mechanisms, including inflammation, cell proliferation, and tissue remodeling. Melatonin (MLT) and its N1- and N2-substituted derivatives are known to exhibit potent antioxidant and anti-inflammatory properties; however, their specific therapeutic mechanisms in wound healing remain largely unexplored. Therefore, this study aimed to investigate the potential wound-healing properties of MLT and its six derivatives using an integrated computational and in vitro validation approach. Potential targets of MLT and its derivatives were screened using SwissTargetPrediction (version 2023 release) and SuperPred (version 3.0), yielding 491 candidate targets. These targets were cross-referenced with the GeneCards (version 5.24.0) database to map their involvement across the four phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. Network interaction models were constructed using Cytoscape (version 3.10.3) and GeneMANIA (version 3.6.0), and pathway enrichment was analyzed using the ShinyGO (version 0.85.1) platform. Enrichment analysis prioritized HIF-1-related signaling as a candidate regulatory axis associated with the predicted targets of melatonin derivatives across the inflammatory, proliferative, and remodeling phases of wound healing. In vitro validation using normal human dermal fibroblasts (NHDFs) demonstrated that all compounds, at non-toxic concentrations, significantly enhanced cell viability, as measured by the MTT assay. Furthermore, wound scratch assays revealed that the N2-bromobenzoyl-substituted derivative (EBMLT) accelerated cell migration, achieving complete wound gap closure within 24 h and outperforming the parent compound. Molecular docking simulations using AutoDock 4.2 predicted favorable binding interactions of the derivatives toward key wound healing-related targets (NF-κB, EGFR, VEGFR-1, MMP-1, and MMP-13). Aromatic-substituted derivatives (BMLT, BBMLT, and EBMLT) exhibited more favorable predicted binding interactions than the parent compound across all targets, whereas the aliphatic-substituted derivative (SMLT) showed weaker predicted interactions, particularly with VEGFR-1. These findings suggest that N1- and N2-aromatic substitutions are associated with more favorable binding interactions. Notably, the N2-bromobenzoyl derivative (EBMLT) exhibited the most potent wound-closure activity, highlighting it as a candidate compound for wound-healing applications. Full article

Introduction: DNA aptamers are single-stranded nucleic acids capable of selectively binding target proteins and have emerged as potential alternatives to antibodies in molecular diagnostics. This study aimed to develop and characterize in silico designed DNA aptamers targeting Interferon alpha-inducible protein 6 (IFI6) and Radical S-adenosyl-L-methionine domain-containing protein 2 (RSAD2) for oral squamous cell carcinoma (OSCC). Methods: Genomic transfer RNA sequences from Homo sapiens, Mus musculus, and Escherichia coli were computationally truncated and optimized to generate DNA aptamer candidates ranging from 35–50 mers. Secondary and tertiary structures were generated using Mfold and RNAComposer, followed by molecular docking with AutoDock Vina and molecular dynamics simulations in GROMACS to evaluate docking interactions and structural behavior comparatively. Selected DNA aptamer candidates were synthesized and evaluated by aptahistochemistry (AHC) to qualitatively explore preliminary tissue reactivity in formalin-fixed paraffin-embedded OSCC tissues under optimized conditions. Results: Molecular docking demonstrated favorable comparative docking scores ranging from −15.6 to −18.7 kcal/mol. RMSD analysis demonstrated that selected IFI6 and RSAD2 DNA aptamer–protein complexes reached a plateau with relatively small fluctuations following maximum RMSD values. In contrast, RMSF analysis identified increased flexibility predominantly within loop regions. Cross-reactivity analysis explored preliminary target selectivity, with no interactions observed within the selected target-binding regions. During AHC optimization, the 50-IFI6 and 45-RSAD2 DNA aptamer candidates exhibited cytoplasmic brown granular staining in >50% of OSCC tumor cells under the optimized experimental conditions. Conclusions: The findings support the applicability of an integrated in silico workflow for generating structurally optimized DNA aptamer candidates and provide preliminary proof-of-concept for their exploratory histopathological application in OSCC. Full article

Purpose: To characterize the messenger RNA (mRNA) and microRNA (miRNA) expression profiles of the normal human cornea and conjunctiva using impression cytology (IC) samples and to investigate their molecular characteristics and regulatory networks. Methods: Corneal and conjunctival IC samples were collected from healthy subjects. Whole-transcriptome and miRNA sequencing were performed, followed by differential expression and bioinformatics analyses. Regulatory networks, protein interaction networks, and functional enrichment analyses were constructed. Selected genes and miRNAs were validated by RT-qPCR. Results: A total of 1676 differentially expressed genes and 175 differentially expressed miRNAs were identified between the cornea and conjunctiva. Functional analyses revealed that genes showing higher expression in the cornea were mainly associated with epithelial structure, barrier function, and antiviral immune responses. In contrast, genes showing higher expression in the conjunctiva were primarily involved in immune regulation, secretion, metabolic detoxification, and tissue remodeling. PPI network analysis showed that hub genes in the cornea were predominantly interferon-stimulated genes related to antiviral responses, while those in the conjunctiva were mainly involved in cell cycle regulation and metabolic detoxification. GO and KEGG analyses further supported these functional distinctions. RT-qPCR validation generally supported the expression patterns identified by RNA sequencing. Conclusions: Our findings reveal that the cornea is characterized by gene expression programs supporting epithelial homeostasis, barrier function, and antiviral immunity, whereas the conjunctiva exhibits transcriptional signatures related to immune surveillance, secretion, metabolic processing, and tissue remodeling. The miRNA–mRNA regulatory networks constructed in this study provide new insights into the molecular regulatory mechanisms of the ocular surface and offer a theoretical basis for future research into disease mechanisms and targeted therapeutic strategies. Full article

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β buildup, tau pathology, neuroinflammation, and declining cognition. Adiponectin, a hormone produced by adipose tissue with insulin-sensitizing, anti-inflammatory, and antioxidant effects, may link peripheral metabolic health to brain function. Studies show that adiponectin helps neurons survive, improves synaptic plasticity, maintains blood–brain barrier integrity, and reduces amyloid-β and tau damage via AdipoR1/R2 signaling. Clinical studies evaluating circulating adiponectin have yielded inconsistent findings, giving rise to the ‘adiponectin paradox’ whereby elevated adiponectin levels in older adults and patients with AD may reflect frailty, weight loss, systemic inflammation, or compensatory responses rather than direct neuroprotective effects. Studies indicate that vitamin D (VD) and L-cysteine (L-Cys), a precursor to glutathione, act synergistically to modulate oxidative stress, inflammation, and adiponectin levels. VD increases circulating adiponectin and benefits metabolism, while L-Cys boosts glutathione, restores redox balance, and promotes adiponectin secretion by affecting fat cell function. Emerging experimental evidence, together with clinical observations from metabolic disorders, suggests that VD and L-Cys may influence adiponectin-related pathways, oxidative stress, and inflammation, which are implicated in AD pathogenesis. However, direct clinical evidence demonstrating that combined VD and L-Cys supplementation modulates these pathways or alters AD progression in humans is currently lacking. This narrative review covers current knowledge of adiponectin and its links to obesity, metabolic issues, and AD, and it also explores the roles of VD and L-Cys as regulators of adiponectin signaling. Overall, the available evidence supports the proposed interaction among VD–L-Cys and adiponectin, which warrants further mechanistic investigation and well-designed clinical studies to determine its therapeutic relevance in AD. Full article

Cervical cancer (CC) affects women worldwide, and more than 95% of cases are caused by persistent infection with high-risk human papillomavirus (HR-HPV), such as type 16, which promotes the progression of precancerous lesions to cancer. This study aimed to identify differentially expressed proteins (DEPs) in biopsies from patients with HPV16+ low-grade squamous intraepithelial lesions (LSILs) and from patients with HPV16+ squamous cell carcinoma (SCC) compared with those from HPV-negative normal cervical tissue (NCT HPV−) controls. The samples were analyzed by high-performance liquid chromatography–tandem mass spectrometry (HPLC-MS/MS) using a data-independent acquisition (DIA) approach. Data processing and differential protein expression analysis were performed with the DIA-NN software (Data-Independent Acquisition Neural Networks), followed by bioinformatics analyses, including Venn diagrams, pathway enrichment, functional interactome, The Cancer Genome Atlas (TCGA)-SCC data integration, and Western blot detection. In total, 1607 DEPs associated with cell adhesion and extracellular matrix proteins were identified in LSILs, whereas 1516 DEPs associated with catalytic and transport activities were identified in SCC; the proteins overexpressed in LSILs (332) were enriched in processes such as metabolism, immune response activation, and stress and cell death responses. In contrast, proteins overexpressed in SCC (205) were associated with the cell cycle, DNA damage, drug metabolism, proteasome degradation, methylation, and immune response. Interaction analyses highlighted proteins related to early proteins 1,5,6 and 7 (E1, E5, E6, and E7). In terms of the two DEPs, S100 calcium binding protein A10 (S100A10/p11) and thymidine phosphorylase (TYMP) were detected in patients with LSIL, HSIL, and SCC at the protein level, consistent with their higher transcript levels in public datasets. Given the small, exploratory cohort, these findings are hypothesis-generating, and validation in a larger, balanced, independent cohort is required. In conclusion, this study identified DEPs associated with the progression of premalignant lesions to SCC that may represent candidate biomarkers and therapeutic targets warranting further investigation. Full article

Objective: Ulcerative colitis (UC) is a relapsing inflammatory disorder of the colon in which persistent mucosal injury, oxidative stress, and defective healing processes contribute to disease progression. Given the need for alternative therapeutic strategies, this study evaluated the efficacy of intrarectal quince gel in an experimental UC model using an integrated approach that combined biochemical assays, histopathological and immunohistochemical examinations, bioinformatic analyses, and molecular docking. Methods: A total of 28 male Wistar albino rats were randomly allocated to one of four experimental groups: Sham, Quince Gel, UC, and UC + Quince Gel (n = 7/group). UC was induced by intrarectal administration of 4% acetic acid, followed by daily intrarectal quince gel treatment for 10 days. To determine the therapeutic effects of quince gel, macroscopic and histopathological changes, colon mass index, oxidative stress indicators (TAS, TOS, OSI, and MDA), serum biochemical parameters, and inflammatory mediators, including TNF-α, IL-1β, and IL-6, were evaluated. TGF-β and FGF expression levels were assessed by immunohistochemistry and quantified using QuPath software (version 0.7.0). The phytochemical composition of quince gel was characterized by LC–MS/MS analysis, while protein–protein interaction network analysis and molecular docking were performed to investigate the potential molecular mechanisms underlying its biological effects. Results: Quince gel significantly alleviated acetic acid-induced colonic injury by reducing macroscopic damage scores, histopathological injury, and colon mass index. Treatment restored oxidative balance by increasing total antioxidant status while decreasing total oxidant status, oxidative stress index, and malondialdehyde (MDA) levels. In addition, serum LDH, CRP, TNF-α, IL-1β, and IL-6 levels were markedly reduced compared with the untreated UC group. Histological examination demonstrated preservation of epithelial integrity, reduced inflammatory cell infiltration, and improved mucosal architecture. Quantitative immunohistochemical analysis showed significant attenuation of TGF-β and FGF overexpression following quince gel treatment. LC–MS/MS identified quercetin as a major bioactive constituent of the gel. Bioinformatic analysis revealed TGFB1, STAT3, and MMP9 as central hub proteins within the UC-associated interaction network, whereas molecular docking demonstrated the strongest binding affinity of quercetin toward TNF-α (−7.379 kcal/mol), supporting its potential anti-inflammatory mechanism. Conclusions: Quince gel exerts significant anti-inflammatory, antioxidant, and mucosal regenerative effects in experimental UC. The integration of histopathological, immunohistochemical, phytochemical, bioinformatic, and molecular docking findings suggests that quince gel may protect colonic tissue through coordinated modulation of oxidative stress, inflammatory cytokines, and tissue repair pathways. These findings support its potential as a promising complementary therapeutic strategy for UC. Full article

TLSs are ectopic, non-encapsulated aggregates of immune cells that develop de novo in non-lymphoid tissues in response to persistent antigenic stimulation and have emerged as clinically relevant features of many solid tumours. However, conventional TLS assessment based on presence/absence, density, or simplified maturation scales does not adequately explain why TLSs are associated with favourable, neutral, or even adverse clinical outcomes across tumour types and treatment settings. In this review, we synthesise the current biological, spatial, and clinical evidence and argue that TLSs should be interpreted not as static histologic findings but as functional immune niches shaped by three interacting axes: structural maturity, spatial localisation, and the functional immune context. We discuss how mature germinal centre-positive TLSs often reflect coordinated B-cell–T-cell cooperation and sustained antigen-driven anti-tumour immunity, whereas partially organised or suppressive TLSs may display transitional or immunoregulatory properties. On this basis, we propose a pragmatic, pathology-oriented conceptual framework that groups TLSs into three simplified functional states: TLS-A, representing mature effector TLSs with germinal centre activity; TLS-B, representing organised but incompletely matured or functionally intermediate TLSs; and TLS-C, representing TLSs dominated by regulatory or suppressive immune programs. We further place these states within recurrent tumour microenvironment archetypes and outline the rationale for a “proposed functional TLS score” integrating histopathologic and molecular readouts. Rather than introducing a definitive biological taxonomy, this framework is intended as a translational model for harmonising TLS interpretation, refining biomarker development, and supporting future studies on prognosis, immunotherapy response, and standardised pathology reporting in solid tumours. Because this framework is derived from a narrative synthesis of published evidence rather than from formal validation, it should be regarded as hypothesis-generating and requires prospective, tumour-specific validation before clinical implementation. Full article

Given the urgent need to regulate oxidative stress microenvironments in chronic wound healing, hydrogel dressings that simultaneously integrate antioxidant, antibacterial, mechanically adaptive, and biocompatible properties are highly desirable. In this study, a natural polymer-based composite hydrogel dressing loaded with zinc-quercetin nanozyme (Zn-Q) was designed. The gel skeleton was constructed via a dual network of photocrosslinked methacrylated silk fibroin (SilMA) and mercaptolated hyaluronic acid (HA-SH) via thiol-ene click chemistry, with the catalase (CAT)-like Zn-Q nanozyme encapsulated in situ within the network, thereby achieving synergy between chemical crosslinking and dynamic metal-polyphenol coordination. Systematic characterization revealed that Zn-Q nanozyme adopted a stable octahedral coordination configuration, and its continuous porous structure exposed abundant catalytically active sites. The composite hydrogels exhibited a highly interconnected, three-dimensional (3D) porous morphology, with swelling ratios that increased significantly with Zn-Q nanozyme content (up to around 1082%). Rheological and mechanical tests demonstrated that although incorporating the nanozyme reduced the storage modulus, the reversible physical crosslinks formed via hydrogen bonding and coordination interactions endowed the material with excellent tensile toughness and energy-dissipation capacity, exhibiting typical Mullins softening behavior. Functional evaluation showed that Zn-Q nanozyme conferred superior free radical scavenging capability to the hydrogels and exerted dose-dependent inhibition against both Staphylococcus aureus and Escherichia coli. Furthermore, the hydrogels exhibited favorable adhesion to various wet organs and heterogeneous material surfaces, with hemolysis rates below 5% and cell viability exceeding 100% after 3 days of culturing with fibroblasts, confirming their excellent hemocompatibility and cytocompatibility. This study provides an experimental basis for developing a new type of wound repair materials that integrate antioxidant, anti-infective, and mechanically adaptive properties, holding significant application potential in oxidative stress-related tissue repair fields. Full article