Materials Today Bio
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2025
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IF 10.2
Haozhe Ren,Peisheng Liu,Ziang Sun,Zhe Yu,Hao Guo,Xinyue Cai,Yihang Wei,Zihan Li,Meiling Wu,Xinyue Xu,Jing Wang,Kun Xuan
Periodontal disease, a chronic inflammatory condition driven by dysbiotic biofilms and host immune dysregulation, lacks therapeutic strategies that simultaneously eliminate infection, resolve inflammation, and promote tissue regeneration. To bridge this gap, we designed a spatially compartmentalized dual-module nanosystem with ‘‘one cerium, dual functions’’. Specifically, the antibacterial module utilizes hyaluronic acid (HA)-modified single-atom cerium nanozymes (Ce-N-C@HA) delivered to periodontal pockets. Upon HA degradation by bacterial hyaluronidase, the exposed catalytic sites generate hydroxyl radicals (·OH) via peroxidase like (POD-like) activity, enabling targeted pathogen eradication. Concurrently, the immunomodulatory module delivers Lactobacillus reuteri -derived extracellular vesicles (EVs) loaded with ultra-small CeO 2 nanoparticles (CeO 2 -EV) into subgingival tissues. This module efficiently scavenges reactive oxygen species (ROS) and induces macrophage polarization to M2 anti-inflammatory phenotype, significantly alleviating the inflammatory microenvironment. By utilizing cerium's dual functionalities which localized antibacterial action and reconstructs immune homeostasis, this system improves the periodontal microenvironment and promotes tissue regeneration, providing a novel strategy for nanotherapy in oral inflammatory diseases.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Dalei Li,Yawen Yu,Rong Fan,Mingyan Yang,Yuxuan Zou,Fei Yao,Yami Wu,Yi Ge,Huaying Fan
Oral ulcers (OU) are prone to recurrence, and are often manifested by the accompanying bacterial infections which may induce a vicious cycle of oxidative stress and inflammatory responses. Traditional treatment methods have limited effects, including being eliminated in the moist and dynamic environment of the mouth, and are prone to various side effects or the development of drug resistance. In this study, we designed borate ester-based and Schiff base-cross-linked hydrogel (OPEC), and loaded ginseng-derived exosome (GEX@OPEC) for the treatment of OU. OPEC hydrogel is composed of phenylboronic acid-functionalized hyaluronic acid oxide (OHA-PBA), epigallocatechin gallate (EGCG), and carboxymethyl chitosan (CMCS). The addition of EGCG enhances its borate cross-linking network and improves the adhesion of the hydrogel. GEX is connected to OPEC through hydrogen bonds and loaded into the hydrogel, further enhancing its gel network. GEX@OPEC exhibited excellent biocompatibility and degradability, ensuring safe oral use of the hydrogel. GEX@OPEC can release EGCG and GEX in response to pH and ROS to exert therapeutic effects. Our research results showed that GEX@OPEC had excellent antibacterial properties, anti-inflammatory and antioxidant stress effects, as well as angiogenic properties, which can effectively promote the healing of OU in diabetic rat models simulating OU. To sum up, GEX@OPEC has good application prospects in the treatment of diabetic OU.
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CHEMICAL ENGINEERING JOURNAL
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2025
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IF 13.2
Haonan Zhang,Huili Zhao,Yingying Liu,Tuo Ji,Yuzhi Gao,Guohua Chen,Yuwei Bian,Zhiwen Zhao,Kun Yu,Xinwei Li,Xuzhu Gao
The treatment of metabolic dysfunction-associated steatotic liver disease (MASLD) remains a major clinical challenge due to its complex pathogenesis, which involves dysregulated lipid metabolism and severe oxidative stress. To address this issue, we produced a novel and multifunctional nanozyme, MOF-818@UDPG/ASGR1, designed for synergistic therapy via dual-channel lipid regulation and potent reactive oxygen species (ROS) scavenging. The nanozyme was synthesized by functionalizing a trinuclear copper-based MOF-818 core, possessing intrinsic superoxide dismutase (SOD) and catalase (CAT) activities, with uridine diphosphate glucose (UDPG) and an asialoglycoprotein receptor 1 (ASGR1) antibody. The surface-conjugated ASGR1 antibody not only facilitated specific hepatocyte targeting but also triggered intracellular signaling pathways, activated liver X receptor α (LXRα), and promoted cholesterol and lipid efflux. Concurrently, the encapsulated UDPG was delivered intracellularly to the Golgi apparatus, where it could bind to and induce the degradation of site-1 protease (S1P), effectively blocking the proteolytic activation of the key lipogenic transcription factor SREBP1c and suppressing de novo lipogenesis. In both cellular and diet-induced murine models of MASLD, MOF-818@UDPG/ASGR1 showed superior efficacy in alleviating hepatic steatosis, reducing oxidative damage, improving serum lipid profile, restoring liver function (ALT/AST), and protecting against hepatocyte apoptosis. Transcriptomic (RNA-seq) and molecular analyses also validated the coordinated activation of LXRα and suppression of SREBP1c, confirming the proposed synergistic mechanism. This study presents a powerful and rationally designed nano-therapeutic strategy that addresses multiple pathological axes in MASLD, offering a promising and integrated treatment approach.
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Journal of Functional Foods
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2024
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IF 3.8
Ya-wen Zhang,Yue-ru Shen,Hong-yu Zhang,Huai-tong Yao,Bing Hu
Sleep is essential to animals with circadian rhythms. Sleep deprivation causes serious pathophysiological consequences, such as DNA damage and oxidative stress. Pyrroloquinoline quinone (PQQ) is a bioactive food ingredient with antioxidant properties. Here, we used zebrafish continuous swimming paradigm sleep deprivation model to investigate the effect of PQQ on DNA damage. We found that DNA damage and neuronal activity increase following sleep deprivation. PQQ pretreatment reduced DNA damage in the zebrafish dorsal pallium. As an antioxidant, PQQ effectively inhibited reactive oxygen species (ROS) production induced by 2,2′-azobis-2-methyl-propanimidamide dihydrochloride (AAPH) and sleep deprivation, and upregulated the expression of antioxidant genes sod1 and gpx4b . Also, PQQ ameliorated the decreased silent information regulator 1 (SIRT1) expression level, suggesting that PQQ may remove excessive ROS by activating SIRT1, thereby reducing DNA damage within neurons. This study indicates that PQQ has strong antioxidant function, provides ideas for further development of ingredients for sleep recovery.
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Pharmaceutics
·
2025
·Vol. 17
·期 7
·940
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IF 5.5
Xin Zhang,Ruonan Lian,Bingbing Fan,Lei Meng,Pengxia Zhang,Yu Zhang,Weitong Sun
Objectives:Colorectal cancer (CRC) is a leading cause of cancer-related mortality, driven by chronic inflammation, gut microbiota dysbiosis, and complex tumor microenvironment interactions. Current therapies are limited by systemic toxicity and poor tumor accumulation. This study aimed to develop a ROS/enzyme dual-responsive oral drug delivery system, KGM-CUR/PSM microspheres, to achieve precise drug release in CRC and enhance tumor-specific drug accumulation, which leverages high ROS levels in CRC and the β-mannanase overexpression in colorectal tissues.Methods:In this study, we synthesized a ROS-responsive prodrug polymer (PSM) by conjugating polyethylene glycol monomethyl ether (mPEG) and mesalazine (MSL) via a thioether bond. CUR was then encapsulated into PSM using thin-film hydration to form tumor microenvironment-responsive micelles (CUR/PSM). Subsequently, konjac glucomannan (KGM) was employed to fabricate KGM-CUR/PSM microspheres, enabling targeted delivery for colorectal cancer therapy. The ROS/enzyme dual-response properties were confirmed through in vitro drug release studies. Cytotoxicity, cellular uptake, and cell migration were assessed in SW480 cells. In vivo efficacy was evaluated in AOM/DSS-induced CRC mice, monitoring tumor growth, inflammatory markers (TNF-α, IL-1β, IL-6, MPO), and gut microbiota composition.Results:In vitro drug release studies demonstrated that KGM-CUR/PSM microspheres exhibited ROS/enzyme-responsive release profiles. CUR/PSM micelles demonstrated significant anti-CRC efficacy in cytotoxicity assays, cellular uptake studies, and cell migration assays. In AOM/DSS-induced CRC mice, KGM-CUR/PSM microspheres significantly improved survival and inhibited CRC tumor growth, and effectively reduced the expression of inflammatory cytokines (TNF-α, IL-1β, IL-6) and myeloperoxidase (MPO). Histopathological and microbiological analyses revealed near-normal colon architecture and microbial diversity in the KGM-CUR/PSM group, confirming the system’s ability to disrupt the “inflammation-microbiota-tumor” axis.Conclusions:The KGM-CUR/PSM microspheres demonstrated a synergistic enhancement of anti-tumor efficacy by inducing apoptosis, alleviating inflammation, and modulating the intestinal microbiota, which offers a promising stimuli-responsive drug delivery system for future clinical treatment of CRC.
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ENVIRONMENTAL POLLUTION
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2025
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IF 7.3
Mengqiang He,Xiaolei Teng,Junyan Wei,Xiaoyu Li,Zunyao Wang
o,p’-dichlorodiphenyltrichloroethane (2,4′-DDT) is a typical persistent organic pollutant (POP) characterized by environmental persistence and acute toxicity. Its pronounced hydrophobicity drives preferential adsorption onto suspended particulate matter (SPM) in aquatic systems. This study systematically investigated the photochemical transformation mechanism of 2,4′-DDT in the Pearl River SPM-water system. Environmental factor analysis revealed negligible effects from pH and cations on 2,4′-DDT photodegradation, while NO 3 − and HCO 3 − inhibited degradation via competitive UV absorption and reactive species quenching. Reaction mechanisms were probed through H 2 O 2 -enhanced hydrophilic reactive oxygen species (ROS) generation, revealing dual photosensitizing and ROS-quenching roles of dissolved organic matter (DOM) in SPM. Hydrophobicity-dependent degradation patterns were revealed through quenching experiments and comparative POPs studies, demonstrating that hydrophilic-region ROS (particularly •OH) contributed dominantly to 2,4′-DDT degradation compared to hydrophobic-region ROS. The LC-MS and GC-MS analyses identified three transformation pathways: dechlorination, elimination, and hydroxylation. Theoretical calculations confirmed C-Cl bond cleavage and elimination feasibility, with •OH attacking benzene-ring carbons at minimal energies, explaining the formation of hydroxylated products. Notably, toxicity assessments revealed enhanced hazards of dechlorination and elimination photoproducts to humans and aquatic organisms than the parent compound.
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BIOMACROMOLECULES
·
2025
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IF 5.4
Qianru Li,Yuhe Zhu,Jiahui Ding,Weizhen Pan,Yuwei Hu,Jiao Lu,Sihai Gao,Hongyang Jiang,Zhongyuan Yin,Songwei Tan
Gene therapy is often limited by gene vectors. To reduce the impact of intracellular reactive oxygen species and improve transfection efficiency, thioether bonds were introduced in poly(β-amino ester) (PBAE), a well-known nonviral gene vector, to synthesize PBAE-poly(β-thioether ester) copolymer (PBAE-TE). By varying the monomer feeding ratio and reaction time, the optimized copolymer (PBAE-TE2–5) showed the highest transfection efficiency in SiHa and HeLa cells (75.00 and 78.70%) with a 75:1 copolymer/GFP ratio. PBAE-TE2–5 also demonstrated superior transfection performance compared to PBAE in multiple cell lines (HeLa, Me180, C666–1, and HEK 293T) and better penetration capability in 3D spheroid cell models (SiHa and HEK 293T). The PBAE-TE2–5-CRISPR/Cas9 plasmid polyplexes could effectively edit target genes in HEK 293T (MUC2) and SiHa (HPV16 E7) cells, and inhibit cancer cell proliferation both in vitro and in vivo. These findings highlight the promising potential of PBAE-TE as an effective gene delivery system.
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Advanced Healthcare Materials
·
2026
·
IF 11
Zhi-Yuan Li,Ying-Ying Han,Qing-Hua Shen,Peng Wang,Long-Bo Yu,Cai-Ping Tan
The hypoxic and immunosuppressive tumor microenvironment limits photodynamic therapy (PDT) and antitumor immunity. To address this, we construct a hypoxia-adaptive nanoplatform PG@Mn-ZIF8 by co-encapsulating a J-aggregating platinum photosensitizer Pt-3T and the nitric oxide (NO) donor S-nitrosoglutathione (GSNO) within Mn 2+ /Zn 2+ doped ZIF-8. This nanoplatform can decompose endogenous H 2 O 2 to O 2 via Pt aggregate-mediated catalase (CAT)-mimetic activity, alleviating hypoxia before light irradiation. Upon illumination, Pt-3T generates a robust Type I/II reactive oxygen species (ROS) storm, which triggers rapid NO release from GSNO, and further convert ROS and NO into highly cytotoxic peroxynitrite (ONOO •− ), thereby amplifying an ROS/RNS storm within the confined MOF space. This co storm disrupts redox homeostasis to induce both necroptosis and ferroptosis alongside immunogenic cell death (ICD). Moreover, the released Mn 2+ and Zn 2+ upon MOF degradation synergistically potentiate the cyclic GMP-AMP (cGAMP) synthase (cGAS)–stimulator of interferon genes (STING) pathway. Consequently, the spatiotemporal “O 2 –ROS/RNS–metal ions” cascade enables the nanoplatform to trigger multimodal cell death and ignite cGAS-STING-driven innate and adaptive immunity, eradicating solid tumors, establishing long-term immune memory, and reversing the “cold” tumor phenotype.
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BIOMATERIALS
·
2026
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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
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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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Nanoscale
·
2026
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IF 5.2
Qinsheng Hu,Shiying Lang,Yangrui Du,Hexin Zhou,Miao Liu,Qiao Jin,Kaijun Li,Gongyan Liu
Frostbite is common in high-altitude regions, where low oxygen levels and the cold climate aggravate wound hypoxia and reactive oxygen species (ROS) accumulation, making frostbite lesions prone to becoming hard-to-heal wounds. Traditional hydrogel dressings remain unsatisfactory under such extreme conditions, as they lack freezing resistance, low-temperature adhesion, sustained oxygen release, and ROS-scavenging activity. Herein, we report a multifunctional hydrogel for the management of high-altitude frostbite wounds, formed from polyvinylpyrrolidone-coated CaO2 nanoparticles (CPO NPs), polyvinyl alcohol, tannic acid (TA), and glycerol through dynamic hydrogen-bonding interactions. The resulting CPO-PTG hydrogel exhibits injectability, rapid gelation, shape adaptability and self-healing, enabling conformal coverage of irregular frostbite wounds. The inclusion of glycerol endows the hydrogel with excellent antifreezing and water-retention properties, while reinforcing multiple covalent and noncovalent interactions between TA within the hydrogel and wound tissues, resulting in strong adhesion even at −20 °C. TA also contributes strong antibacterial activity, helping prevent wound infection. Notably, the hydrogel network regulates oxygen release from CPO NPs to achieve sustained oxygen delivery for 12 days and, together with the ROS-scavenging activity of TA, promotes cell proliferation and tube formation in vitro under hypoxic conditions. In a rat frostbite-induced hypoxic wound model, CPO-PTG hydrogel accelerates wound healing by reducing inflammation and enhancing angiogenesis. Therefore, this multifunctional hydrogel offers a promising strategy for frostbite wound repair, with potential applicability to other hypoxic wounds in high-altitude settings.
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ANTIOXIDANTS & REDOX SIGNALING
·
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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