ACS Applied Materials & Interfaces
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2025
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IF 8.2
Shuying He,Yuerong Lv,Jingnan Qiu,Shudan Cui,Zixian Gao,Liang Peng
Treating metabolic dysfunction-associated fatty liver disease (MAFLD) and reducing the occurrence of MAFLD-associated liver cancer remain challenging. Two-dimensional (2D) tantalum carbide (Ta4C3) MXene nanozymes (MXenzymes) exhibit antioxidant and anti-inflammatory activities and have thus attracted considerable attention in the fields of oncology and engineering. However, the potential mechanism of action and bioactive properties of Ta4C3 in MAFLD remain uncertain. In our study, Ta4C3 not only inhibited lipid accumulation and disrupted lipid metabolism in hepatocytes but also reduced cell death caused by fatty acids by decreasing intracellular reactive oxygen species (ROS) levels, which significantly promoted the polarization of M1 macrophages to M2 macrophages by alleviating oxidative stress and further suppressing inflammatory factor expression. In mice fed a methionine–choline-deficient (MCD) diet, Ta4C3 reduced lipid accumulation, the infiltration of inflammatory cells, and liver cell apoptosis by modulating the cellular microenvironment through its anti-inflammatory and antioxidant properties. Therefore, Ta4C3 can be used as a multifunctional bioactive material to alleviate hepatic steatosis and inflammation in individuals with MAFLD/metabolic dysfunction-associated steatohepatitis (MASH) because of its robust antioxidant and anti-inflammatory effects.
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CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Yi Yao,Zixin Gao,Zhongjie Pan,Yanping Zhong,Lili Qin,Kexin Zhao,Shuhan Liu,Shengqing Zhang,Haoyang Han,Feiying Yin,Ruizheng Liang,Jinmin Zhao,Li Zheng
Platinum (Pt)-based nanozymes that effectively exert antioxidant effects exhibit great potential in the treatment of osteoarthritis (OA). However, these nanozymes are easy to agglomerate and have low catalytic efficiency, which can hardly meet the criterion of clinical therapy. To achieve efficient ROS removal, this study develops a novel ultrasound (US)-responsive piezoelectric nanozyme (MOF(Hf)-Pt) based on Pt with multi-enzyme mimicking activities and metal-organic frameworks (MOFs) with excellent piezoelectric properties. Results show that MOF(Hf)-Pt has excellent piezocatalytic enzyme activity, which can be adjusted by varying the intensity and time of US. Mechanistically, MOF(Hf)-Pt can increase ATP output and restore mitochondrial function, thereby reducing inflammatory factor levels. In vivo studies also reveal that under suitable US action, MOF(Hf)-Pt nanozymes can effectively inhibit the deterioration of OA, with reductions in OARSCI scores of 76.90 % and 82.66 % after 4 and 8 weeks, respectively. Particularly, the piezoelectric catalytic effect generated by MOF(Hf)-Pt can reverse oxidative stress-induced articular cartilage damage and promote cartilage regeneration, making it a promising candidate for OA treatment.
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ACTA PHARMACOLOGICA SINICA
·
2025
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IF 8.4
Mu Wei,Shi Ya-ge,Jian Yu-lun,Li Lei,Zhou Yan-feng,Wang Hui,Ge Yang
The progression of hepatocellular carcinoma (HCC) is partly driven by reactive oxygen species (ROS)-induced tissue damage and inflammation. Nicotinamide adenine dinucleotide phosphate oxidases (NOXs) are key regulators of ROS production, yet the specific role of NOX1 in HCC progression and therapeutic response remain incompletely understood. In this study we investigated the critical role of NOX1 in progression, metastasis and therapeutic sensitivity of HCC, and explored its potential as a therapeutic target. By comprehensive analysis of public databases and validation with in-house clinical specimens, we showed that NOX1 expression was significantly elevated in metastatic HCC that was correlated to poor patient prognosis. Knockdown of NOX1 or pharmacological inhibition with a selective NOX1 inhibitor ML171 significantly reduced ROS production and suppressed HCC cell motility and invasion in vitro. NOX1 inhibition also attenuated HCC metastasis in experimental metastasis mouse model using direct injection of HCC cells, and mitigated CCl 4 -induced liver injury and pro-tumorigenic microenvironment in CCl 4 -induced chronic liver injury and spontaneous tumor development mouse model. Importantly, we demonstrated that combined sorafenib or radiotherapy with NOX1 inhibition synergistically reduced the metastatic potential of HCC cells and enhanced the therapeutic efficacy. Bioinformatics analysis revealed that NOX1 contributed to HCC metastasis and therapy resistance by modulating ROS homeostasis, cellular antioxidant systems and inflammatory pathways. Taken together, this study elucidates the critical role of NOX1 in HCC pathogenesis, suggesting that NOX1 inhibition represents a promising strategy to overcome resistance and enhance HCC sensitivity to sorafenib and radiotherapy.
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Advanced Composites and Hybrid Materials
·
2025
·Vol. 8
·期 4
·1-23
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IF 21.8
Yin Xiujuan,Xue Shuqin,Ji Jiaqi,Zhao Mingyu,Shao Min,Yin Likang,Zhang Saisai,Liu Lei,Li Bin,Zhang Lei,Li Yuan,Wang Xiao
Liver fibrosis (LF) is a leading cause of liver-related mortality worldwide. Although antifibrotic drugs are commonly used in clinical practice, their efficacy remains limited. Excessive reactive oxygen species (ROS) in the fibrotic liver microenvironment play a crucial role in LF progression. Nanozymes, owing to their enzyme-mimicking catalytic activity and antioxidant properties, offer a promising strategy for LF treatment. Vanadium-based nanozymes exhibit ROS-scavenging capabilities and promote fibrosis reversal, while zirconium (Zr)-based metal–organic frameworks (MOFs), such as UiO-66, possess excellent biocompatibility and catalytic activity. However, the therapeutic efficacy of nanozymes is hindered by their intrinsic catalytic limitations. Ultrasound (US), a non-invasive therapeutic modality, has been shown to enhance nanozyme activity and improve treatment outcomes. In this study, we developed a dual-nanozyme composite (UiO-66/V 2 C/L-Arg/pPB, UVLp) with targeted ROS-scavenging and L-arginine (L-Arg) delivery capabilities. Upon ultrasound exposure, UVLp releases L-Arg and nanozymes, facilitating nitric oxide (NO) generation, alleviating oxidative stress, and mitigating liver fibrosis. This work introduces a novel ultrasound-activated nanozyme platform for LF therapy, providing valuable insights for clinical translation.
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Small
·
2025
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IF 12.1
Xinyue Guo,Hongru Li,Yu Chen,Zongjia Li,Miaomiao Zhang,Jinyao Zheng,Jiang Li,Xiue Jiang,Jilin Tang
The treatment of persistent drug-resistant bacterial infections in wounds poses a significant global medical challenge. Developing innovative antimicrobial strategies capable of simultaneously achieving bacterial eradication, inflammation resolution, and tissue regeneration has become imperative. Herein, a nanocomposite featuring plasma-enhanced enzymatic activity and immunoregulatory properties is engineered, designed to reprogram the wound microenvironment and expedite healing in drug-resistant bacterial infections. Capitalizing on the localized surface plasmon resonance effect of Au@Ag nanoparticles coupled with the pH-dependent peroxidase-like (POD-like) activity of cerium dioxide (CeO 2 ), the BSA-(Au@Ag/CeO 2 ) nanocomposites orchestrate dual-modality photothermal-chemodynamic therapy for enhanced bactericidal efficacy and biofilm disruption. Upon near-infrared laser irradiation, plasmon-generated hot electrons are transferred to CeO 2 , triggering massive reactive oxygen species production via enhanced POD-like catalysis. This synergistic dual-action mechanism eradicates methicillin-resistant Staphylococcus aureus (MRSA) through membrane disruption and reactive oxygen species (ROS)-induced oxidative stress. Remarkably, the nanosystem not only suppresses proinflammatory cytokine storms but also steers macrophage polarization toward tissue reparative M2 phenotypes at infection sites, thereby alleviating pathological inflammation and fostering regenerative microenvironments. Biosafety assessments confirm the absence of discernible toxicity in vital organs. This multifunctional platform represents a paradigm-shifting strategy for managing antibiotic-resistant wound infections, providing a clinically translatable solution to combat antimicrobial resistance.
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ACS Nano
·
2022
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IF 18.027
Shanshan Liu,Bingnan Wang,Yuewen Yu,Yubo Liu,Zeyan Zhuang,Zujin Zhao,Guangxue Feng,Anjun Qin,Ben Zhong Tang
Photodynamic therapy as an emerging phototheranostic approach holds great potential for antibacterial treatment, but is limited by compromised reactive oxygen species (ROS) generation in an aggregate and hypoxic microenvironment. Herein, we report a molecular cationization approach to boost the ROS, especially type I ROS generation of aggregation-induced emission (AIE) photosensitizers for photodynamic treatment of drug-resistant bacteria. Such cationization reinforces the electron-accepting ability of the cationic moiety, promotes intersystem crossing (ISC), and increases electron separation and transfer processes. The resultant CTBZPyI exhibits largely enhanced ROS generation ability with predominant hydroxyl radical generation over its neutral counterpart in aggregate. Moreover, cationization also confers CTBZPyI with the bacterial binding ability and a moderate bacterial inactivation ability in the dark. Further light irradiation leads to superb antibacterial performance, which largely promotes the healing process of a MRSA-infected wound. Such a cationization strategy is expected to be a general strategy for the design of highly effective type I photosensitizers for bacterial infection treatment.
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JOURNAL OF CONTROLLED RELEASE
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2024
·
IF 10.5
Huijuan Zhang,Jingjing Wang,Yingmei Tian,Chaoqun Wang,Lin Hou
The ischemic strokes seriously threaten human health with high incidence and disability rates. Cerebral embolism and impaired brain function are the two major clinical features of this disease. Therefore, rapid restoration of cerebral blood supply and synchronous improvement of impaired neurological function is the key to treating strokes. Herein, based on the microenvironment of cerebral thrombosis and pathological characteristics of damaged neurons, we constructed a shear force and reactive oxygen species (ROS) dual-responsive system (UK@Fuc/CDPC-PTPCS) for sequential targeted delivery of thrombolytic agent urokinase (UK) and neuroprotective drug cytosolic choline (CDPC). Results proved that after intravenous administration, UK@Fuc/CDPC-PTPCS can quickly locate to cerebral thrombosis site via the active recognition capability of fucoidan (Fuc) to P-selectin overexpressed on activated platelets. Subsequently, the sharply increased blood shear force separated the core-shell structure by breaking the host-guest interaction of β-cyclodextrin (β-CD), so the UK loaded in the shell was first released to rapid thrombolysis and then restored cerebral blood supply. Afterward, the stroke homing peptide (SHp) modified CDPC-PTPCS core actively recognized ischemic damaged neuronal cells. Then high intracellular ROS triggered CDPC release at specific sites to exert neuroprotective effects. This study offered a new therapeutic strategy for ischemic stroke.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
You Huang,Pei Wang,Pengyu Zhao,Weijian Cheng,Hao Fu,Xiao Zheng,Lin Chen,Wenyi Huang,Jiajia Xu,Chaomei Fu,Zhen Zhang,Xiao Wang
Patchouli essential oil (PEO) is acknowledged as a potent contender for the management of ulcerative colitis (UC). However, the limited ability of PEO to be absorbed by the body and its low stability substantially limit its potential uses. Furthermore, UC lesions are mainly concentrated in the rectal and colonic mucosa, with excessive production of reactive oxygen species (ROS). Herein, a nanoemulsion of PEO (PEONE) was developed to enhance the stability and bioavailability of a drug. Subsequently, we developed a novel platform for the rectal administration of a ROS/thermo dual-sensitive Bletilla striata polysaccharide-based hydrogel (RTH) co-loaded with PEONE to efficiently treat UC. As expected, the sol–gel transition of PEONE@RTH, after its intrarectal administration, resulted in its extended presence in the colon and facilitated its attachment to the inflammation site. Moreover, PEONE@RTH alleviated dextran sulfate sodium-induced UC symptoms by suppressing inflammation and oxidative stress, repairing the damage to the intestinal epithelial barrier (claudin-1 and occludin), increasing short-chain fatty acid content and inhibiting the MAPK signalling pathway. Additionally, PEONE@RTH exhibits exceptional safety and biocompatibility. Thus, PEONE@RTH has the potential to provide a novel approach for treating UC and other intestinal disorders characterised by similar clinical conditions.
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CHEMICAL ENGINEERING JOURNAL
·
2025
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IF 13.2
Liang Song,Weiwei Zheng,Shuqin Wang,Zihe Zhai,Shifen Li,Jie Ding,Liyin Shen,Jinyue Zhang,Yang Zhu,Changyou Gao
Pathology of myocardial infarction (MI) undergoes continuous spatiotemporal transformation, during which immediate elevated reactive oxygen species (ROS) and subsequent upregulated connective tissue growth factor (CTGF) exacerbate the impairment of cardiac functions. The major challenge lies in designing biomaterials that can adaptively respond to the temporal changes in the MI microenvironment. Herein, we prepared ROS-responsive dual drug-loaded core–shell microgels (SaB/Cand@C-S MGs) using microfluidic chip technology. The hydrogel shell was made from ROS-eliminating hyperbranched poly(acrylate-capped thioketone-containing ethylene glycol) (HBPAK) and methacrylated hyaluronic acid (HAMA), which was further encapsulated with hydrophilic salvianolic acid B (SaB). The oleogel core was loaded with hydrophobic candesartan (Cand). This structure enabled programmed drug release by utilizing ROS-responsive shell. The release of Cand from the SaB/Cand@C-S MGs in vitro was significantly accelerated in the presence of H 2 O 2 , reaching to 68% over 21 d, compared to 24% in PBS. In a rat MI model, minimally invasive injection of the SaB/Cand@C-S MGs into the infarcted area demonstrated both short-term anti-inflammatory effect and long-term benefit in fibrosis suppression. This phase-targeted approach ultimately resulted in improved cardiac functions, reduced fibrosis, and decreased ventricular dilation. The core–shell microgels as a drug reservoir offer a programmed drug delivery strategy adaptive to the specific phases of MI, showing great potential for applications.
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ACS Applied Materials & Interfaces
·
2024
·
IF 8.3
Nan Hu,Meng Sun,Nan Lv,Yangyang Gao,Xiaohong Fu,Dayi Xing,Xiang Guo,Shaodong Zhai,Ruiping Zhang
Myocardial infarction (MI) is the leading cause of death worldwide. The most effective way to treat myocardial infarction is to rescue ischemic cardiomyocytes. After an ischemic event, the overproduction of reactive oxygen species (ROS) is a key driver of myocardial injury. The produced ROS affects mitochondrial function and induces apoptosis in cardiomyocytes. This was accomplished by constructing platelet-membrane-encapsulated ROS-responsive drug-releasing nanoparticles (PMN@NIC-MalNPs) to deliver malonate and niclosamide (NIC). The results revealed that PMN@NIC-MalNPs degraded and released malonate and niclosamide in a high-level ROS microenvironment, effectively reducing the oxidative stress and apoptosis rate. By enhancing basal mitochondrial oxygen consumption rate (OCR), adenosine triphosphate (ATP) production, and spare respiratory capacity (SRC) in vitro, reduced the oxidative stress levels and restored mitochondrial function. In vivo studies revealed that the PMN@NIC-MalNPs improved cardiac dysfunction, inhibited succinate dehydrogenase (SDH) activity, increased ATP production, and reduced the myocardial infarct size in myocardial infarction model mice. Further, transcriptome analysis and Western blot revealed that PMN@NIC-MalNPs prevented apoptosis by activating the expressions of the signal transducer and activator of transcription 3 (STAT3) and Bcl-2, and inhibiting the expression of Bax. Thus, this study provides a novel therapeutic solution for treating myocardial infarction and predicting the viability of an antioxidant and antiapoptotic therapeutic solution in the treatment of myocardial injury.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2024
·
IF 10.6
Wenjie Xu,Zhaokui Zeng,Yucheng Tang,Jingjing Tian,Xinyan Hao,Pengcheng Sun,Yanjin Peng,Tian Tian,Daxiong Xiang,Rongrong Wang,Chuanpin Chen,Junyong Wu
Chemotherapy is still one of the major approaches in triple-negative breast cancer (TNBC) treatment. The development of new formulations for classic chemotherapeutic drugs remains interests in studies. Camptothecin (CPT) is powerful antitumor agents in TNBC treatment though its clinic applications are limited by its low water solubility and systemic toxicity. To prepare a spatiotemporal controllable CPT nano-formulation, we construct a ROS-responsive self-assembly nanoparticle by combining hydrophobic CPT and hydrophilic 5-floxuridine (FUDR). A ROS-sensitive thioketal (TK) linker is used to prepare CPT-TK-FUDR (CTF). Next, we introduced IR780-based phototherapy to elicit massive ROS regeneration due to the endogenous ROS is not sufficient. IR780 is modified with hyaluronic acid (HA) to prepare HA-modified IR780 (HAIR) for its biocompatibility and tumor targeting ability improvement. CTF and HAIR self-assemble to form an attractive nano-bomb (HAIR/CTF NPs). HA accurately guides the NPs to tumor sites via HA-receptor recognition on tumor cells. After internalization, overexpressed intracellular HAase in tumor cells disassembles the NPs to free the contents. Due to the presence of IR780 molecules, the scheduled irradiation of 808 nm laser induces massive reactive oxygen species (ROS) generation, which further result in the cleavage of TK linker for free drugs release. Additionally, ROS-mediated photodynamic therapy (PDT) and near-infrared laser-mediated photothermal therapy (PTT) synergistically worked to eradicate tumor cells. Then immunogenic cell death (ICD) was evoked by CPT and phototherapy to amplify antitumor immunity, thereby achieving primary and abscopal tumor inhibition. In conclusion, the HAIR/CTF nano-bomb realized spatiotemporal controllable drug release, exciting tumor eradication and attractive anti-metastasis efficacy via combination chemo/photo/immunotherapy, offering a valuable reference for the re-development of classic drug in future clinical practice.
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2025
·
IF 6.1
Xianhua Zhang,Runfa Wu,Fasheng Liu,Min Huang,Xiaoyan Huang,Nannan Wang,Qianqian Huang,Minhong Zhang,Xinjun Liao,Huiqiang Lu,Lan Liao
The combustion of biomass (e.g., wood, agricultural residues) and coal releases significant amounts of guaiacol (GUA) and its derivatives, major constituents of PM2.5 that threaten human health and ecosystems. GUA can rapidly enter the Earth's water circulation system through atmospheric deposition. However, its potential threat to aquatic organism and humans remains poorly understood. Using zebrafish—a model organism with high genetic homology to humans, transparent embryos, and rapid development—we investigated GUA’s ecological effects. Zebrafish embryos were exposed to 0.08–0.24 mM GUA from 12 to 120 h post-fertilization (hpf). GUA induced craniofacial malformations, behavioral abnormalities (reduced locomotion, impaired stimuli response), and oxidative stress via reactive oxygen species (ROS) accumulation. Disrupted migration, proliferation, and differentiation of cranial neural crest cells (NCCs) were observed, alongside altered Wnt signaling pathway gene expression. Both astaxanthin (AST, an ROS scavenger) and C59 (a Wnt inhibitor) could mitigate craniofacial defects. These findings demonstrate that GUA reduces antioxidant capacity, impairs NCCs function, and disrupts Wnt signaling, leading to craniofacial deformities. This study highlights GUA’s ecological and health risks, providing insights into its toxic mechanisms.
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