ADVANCED MATERIALS
·
2025
·
IF 26.8
Zekun Wang,Fangyuan Chen,Zhongkun Wang,Mengru Wu,Man Jiang,Zhekang Zheng,Yingying Li,Qing Li,Qingqing Wang,Dongdong Sun,Qingqing Miao
Nanozyme-driven ferroptosis provides a promising therapeutic strategy against drug-resistant bacterial infections by inducing iron overload and oxidative stress. However, bacterial metal transport proteins (MTP) and antioxidant systems can reduce iron accumulation and lipid peroxidation, limiting the efficacy of ferroptosis-based therapies and promoting resistance. Single-atom and chiral nanozymes, with their high atomic utilization and catalytic specificity, may provide an effective approach to overcoming bacterial defense mechanisms, which has been not exploited. In this study, we report D-chiral single-atom iron–carbon dot nanozymes (DFe-NSC) for effective bacterial infection treatment. Compared to L-chiral form (LFe-NSC), DFe-NSC exhibits significantly higher peroxidase (POD)-like and glutathione peroxidase (GPx)-like activities. The enhanced catalytic activity promotes reactive oxygen species (ROS) generation and glutathione depletion, disrupting bacterial redox homeostasis. More intriguingly, DFe-NSC more effectively modulates the expression and iron-regulatory function of MTP (including Fur and FtnA) than LFe-NSC. This will induce substantial accumulation of Fe 2 ⁺ intracellularly and thereafter lipid peroxidation, thereby facilitating the bactericidal effects of ferroptosis-like cell death. Resultantly, DFe-NSC exhibit markedly enhanced antibacterial and antibiofilm activities in diabetic infected wound and osteomyelitis models. This study introduces a chiral catalysis–MTP regulation strategy to induce bacterial ferroptosis-like death, providing a promising alternative for drug-resistant infection treatment.
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Nanomaterials
·
2025
·Vol. 15
·期 19
·1465
·
IF 4.3
Nannan Zheng,Yulan Zhang,Chunlei Dong,Zhiming Chen,Jianbin Chen
Fe–porphyrin/g-C3N4composites have emerged as promising visible-light photocatalysts, but their performance remains limited by inefficient charge separation and low reactive oxygen species (ROS) yield. Here, iron–tetra(4-carboxyphenyl) porphyrin (Fe–TCPP) was coupled with g-C3N4nanotubes (CNNTs) via a facile self-assembly strategy, creating a morphology-coordinated system. Comprehensive characterization (XRD, FTIR, SEM/TEM, BET, UV–Vis diffuse reflectance, PL, XPS, and EPR) confirmed the structural integrity, electronic coupling, and ROS generation capability of the composites. Fe–TCPP incorporation narrowed the bandgap from 2.78 to 2.56 eV, prolonged the average carrier lifetime from 6.3 to 7.5 ns, and significantly enhanced the generation of •OH and1O2. The optimized 1 wt% Fe–TCPP@CNNTs achieved complete Rhodamine B degradation within 30 min under visible light, with the highest two-stage apparent rate constants (k1= 0.0964 min−1, k2= 0.328 min−1). In addition, the hybrids retained over 90% activity after six consecutive runs, confirming their stability and recyclability. The synergistic effect of Fe–N coordination and nanotubular architecture thus promotes light harvesting, charge separation, and ROS utilization, offering a promising design principle for high-performance photocatalysts in environmental remediation.
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FOOD CONTROL
·
2025
·
IF 6.3
Xianrui Chen,Lin Wang,Lihong Lin,Nitong Bu,Di Zhang,Zhenzhen Wu,Wei Liu,Jie Pang
The development of advanced antimicrobial packaging is crucial for ensuring food safety. This paper reports a novel photodynamic antibacterial film (PVA-CM@TFQ) that effectively combats microbial contamination, delays food spoilage and minimizes the risk of foodborne diseases transmission. Quercetin (Que) was encapsulated within a tannic acid-ferric ion (TA–Fe 3+ ) coordination network and embedded into a biodegradable polymer matrix composed of polyvinyl alcohol (PVA) and carboxymethyl chitosan (CM). The TA-Fe 3+ network significantly improved the stability of Que, while the resulting PVA-CM@TFQ demonstrated excellent mechanical properties, barrier performance, and biocompatibility. Upon light irradiation, the film produced reactive oxygen species (ROS), exhibiting potent photodynamic antibacterial activity, with inhibition rates of 99.83%, 99.42%, 100%, and 100% against Escherichia . coli, Staphylococcus . aureus , Candida. albicans , and Saccharomyces cerevisiae , respectively. When applied to raspberries, hawthorn, goldenberries, and lime, the film effectively prolonged shelf life by suppressing microbial proliferation, minimizing weight loss, and maintaining fruit firmness. These findings highlight a sustainable, light-responsive strategy for fruit preservation with significant potential in enhancing food safety.
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Regenerative Biomaterials
·
2025
·
IF 8.1
Ding Jiaxin,Gao Binbin,Sang Zelin,Dai Zhen,Chen Zhenhua,Mei Xifan
Spinal cord injury (SCI) is a kind of health problem characterized by oxidative stress and neuronal apoptosis, which pose major challenges to the recovery of patients. Recently, the application of photothermal nanotechnology in medicine has opened up exciting new avenues for the treatment of SCI. This innovative approach leverages the unique properties of nanomaterials to enhance therapeutic outcomes. In our study, we developed a novel nanotherapeutic system named ZnO-ZIF8@H, which is designed to deliver targeted neuroprotective effects. We meticulously evaluated its performance under near-infrared (NIR) irradiation, which is known to promote local heating and stimulate biological processes. The data indicated that the application of ZnO-ZIF8@H combined with NIR irradiation significantly reduced oxidative stress levels in the affected tissues. This was evidenced by a marked decrease in malondialdehyde (MDA) levels, a well-known indicator of lipid peroxidation and cellular damage. Simultaneously, the treatment notably enhanced the activity of superoxide dismutase (SOD) and glutathione (GSH) enzymes. These findings suggest that ZnO-ZIF8@H+NIR could both protect cells from oxidative damage and boost the internal antioxidant defenses, highlighting its potential as an effective therapeutic strategy for mitigating secondary injuries following spinal cord trauma. It also suppressed neuronal apoptosis, as evidenced by TUNEL staining and decreased Cleaved-Caspase3 expression in NeuN-positive neurons. These results indicated that ZnO-ZIF8@H+NIR effectively reduces secondary damage from SCI by alleviating apoptosis and oxidative stress, offering a promising approach for the therapy of SCI.
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CHEMICAL ENGINEERING JOURNAL
·
2024
·
IF 13.3
Liangmin Fu,Shan Wang,Na Zhang,Yajing Lin,Shihui Zhang,Yingji Mao,Pinghui Zhou
Mitochondrial dysfunction and redox imbalance in senescent cells hinder bone repair during aging. Thus, strategies to restore mitochondrial function and reduce reactive oxygen species (ROS) levels could effectively counteract cellular senescence and promote osteogenesis. In this study, we developed a Chondroitin Sulfate Methacryloyl (ChSMA) composite hydrogel scaffold (TPG@ChSMA) incorporating tea polyphenol-reduced graphene (TPG). The mitochondrial-targeted antioxidant TPG served as a crucial agent to balance ROS levels and enhance mitochondrial function in senescent cells, while ChSMA promoted bone formation regulation and provided a stabilized ossification platform. The mitochondrial-targeted composite scaffold mediated ROS elimination and counteracted cellular senescence via the SIRT1/PI3K/AKT pathway in vitro . Therefore, it played a pivotal role in maintaining cellular homeostasis by reducing oxidative stress and promoting cell survival. Concurrently, the ERK1/2 pathway was activated to facilitate bone differentiation. The combined activation of these pathways created a microenvironment conducive to regeneration that significantly enhanced the osteogenic differentiation potential of senescent BMSCs. The TPG@ChSMA scaffold demonstrated significant efficacy in promoting bone regeneration and reducing the expression of senescence-associated marker p16 in an osteoporosis rat model induced by bilateral ovariectomy. Overall, these findings underscore the potential of mitochondrial-targeted therapeutic strategies to repair aging bone defects by mitigating ROS levels and alleviating cellular senescence.
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TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2025
·
IF 3.4
Yanan Xia,Lihua Feng,Yuzhi Lan,Xiangxiang Chen,Xiaomin Tang,Hengyi Xu,Yang Liu
Children's daily exposure to titanium dioxide nanoparticles (TiO₂ NPs) poses significant risks to the developing testes, yet few studies have examined their impact on young testicular growth. Given ghrelin's established antioxidant and testis-protective effects in animal models, we hypothesized that it could mitigate TiO₂ NPs–induced damage. In this first systematic investigation of young testicular responses, three-week-old male rats received oral gavage of TiO₂ NPs (100, 200, or 400 mg/kg), followed 30 min later by intraperitoneal ghrelin (50 mg/kg) for four weeks. Exposure to TiO₂ NPs disrupted seminiferous tubule architecture and reduced serum levels of key developmental and sex hormones, including IGF-1, FSH, LH, and testosterone. Mechanistically, TiO₂ NPs activated the ROS/AMPK/mTOR signaling pathway, resulting in a marked reduction of SOD, CAT, and GSH activities and the induction of oxidative imbalance, while simultaneously upregulating the autophagy protein ULK1 and autophagy-related genes to trigger excessive autophagy, ultimately compromising testicular architecture and function. We further assessed ghrelin's protective efficacy against TiO₂ NPs-induced reproductive injury in young rats, demonstrating that ghrelin inhibited the ROS/AMPK/mTOR signaling pathway, attenuated oxidative stress, and suppressed excessive autophagy, thereby mitigating testicular injury. These findings represent the first evidence of the developing testicular heightened vulnerability to TiO₂ NPs toxicity and underscore ghrelin's potential as a novel protective intervention. Our study provides new insights into the reproductive toxicology of engineered nanoparticles and supports targeted strategies to safeguard pediatric reproductive health.
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Cell Death & Disease
·
2021
·Vol. 12
·期 1
·1-18
·
IF 8.469
Fang Shaohong,Wan Xin,Zou Xiaoyi,Sun Song,Hao Xinran,Liang Chenchen,Zhang Zhenming,Zhang Fangni,Sun Bo,Li Hulun,Yu Bo
Inducing autophagy and inhibiting apoptosis may provide a therapeutic treatment for atherosclerosis (AS). For the treatment of progressive AS, arsenic trioxide (ATO) has been used to coat vascular stents. However, the effect of ATO on autophagy of macrophages is still unknown. Therefore, the aims of this study were to characterize the effects and the mechanism of actions of ATO on autophagy in macrophages. Our results showed that ATO-induced activation of autophagy was an earlier event than ATO-induced inhibition of the expression of apoptosis markers in macrophages and foam cells. Nuclear transcription factor EB (TFEB) prevents atherosclerosis by activating macrophage autophagy and promoting lysosomal biogenesis. Here, we report that ATO triggered the nuclear translocation of TFEB, which in turn promoted autophagy and autophagosome-lysosome fusion. Both the latter events were prevented by TFEB knockdown. Moreover, ATO decreased the p-AKT and p-mTOR in the PI3K/AKT/mTOR signaling pathway, thus inducing autophagy. Correspondingly, treatment with the autophagy inhibitor 3-methyladenine (3-MA) abolished the autophagy-inducing effects of ATO. Meanwhile, PI3K inhibitor (LY294002) and mTOR inhibitor (rapamycin) cooperated with ATO to induce autophagy. Furthermore, reactive oxygen species (ROS) were generated in macrophages after treatment with ATO. The ROS scavenger N-acetyl-1-cysteine (NAC) abolished ATO-induced nuclear translocation of TFEB, as well as changes in key molecules of the AKT/mTOR signaling pathway and downstream autophagy. More importantly, ATO promoted autophagy in the aorta of ApoE −/− mice and reduced atherosclerotic lesions in early AS, which were reversed by 3-MA treatment. In summary, our data indicated that ATO promoted ROS induction, which resulted in nuclear translocation of TFEB and inhibition of the PI3K/AKT/mTOR pathway. These actions ultimately promoted macrophage autophagy and reduced atherosclerotic lesions at early stages. These findings may provide a new perspective for the clinical treatment of early-stage atherosclerosis and should be further studied.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2024
·
IF 7.7
Zhuwei Wang,Qinqiu Zhang,Danka Bukvicki,Yi Xu,Yue Peng,Fan Li,Qing Zhang,Shuxiang Liu,Jing Yan,Shang Lin,Wen Qin
Okra is susceptible to browning during storage. The effects of konjac glucomannan/microcapsule of thymol edible coating (TKL) on antioxidant activity and reactive oxygen (ROS) synthesis of okra during low-temperature storage were investigated. Thymol edible coating of thymol concentration 40 mg/mL (TKL40) had a regulatory effect on okra browning. After 14 days of storage, compared with the control group, the weight loss rate of TKL was reduced by 5.26 %, the hardness was increased by 24.14 %, and the L ⁎ value was increased by 31 %. Moreover, TKL40 increased the scavenging capacity of okra for DPPH and ABTS free radicals, and activated catalase and superoxide dismutase activities by promoting the accumulation of total phenolics and flavonoids. TKL40 also reduced the cell membrane damage of okra during low-temperature storage by reducing the increase of malondialdehyde and H 2 O 2 during okra storage. Meanwhile, it delayed the increase of relative conductivity and the production of O 2 .- , inhibited the activity of polyphenol oxidase in the late stage, so reduced the combination of polyphenol oxidase and phenolics to reduce the browning. Therefore, TKL40 reduces okra pericarp browning by regulating antioxidant activity and ROS synthesis.
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ENVIRONMENTAL POLLUTION
·
2020
·
IF 6.793
Caiying Zhang,Tianjin Lin,Gaohui Nie,Ruiming Hu,Shaoxing Pi,Zejing Wei,Chang Wang,Chenghong Xing,Guoliang Hu
Cadmium (Cd) and excess molybdenum (Mo) are harmful to animals, but the combined nephrotoxic mechanism of Cd and Mo in duck remains poorly elucidated. To assess joint effects of Cd and Mo on pyroptosis via ROS/PTEN/PI3K/AKT axis in duck renal tubular epithelial cells, cells were cultured with 3CdSO 4 ·8H 2 O (4.0 μM), (NH 4 ) 6 Mo 7 O 24 ·4H 2 O (500.0 μM), MCC950 (10.0 μM), BHA (100.0 μM) and combination of Cd and Mo or Cd, Mo and MCC950 or Cd, Mo and BHA for 12 h, and the joint cytotoxicity was explored. The results manifested that toxicity of non-equitoxic binary mixtures of Mo and Cd exhibited synergic interaction. Mo or/and Cd elevated ROS level, PTEN mRNA and protein levels, and decreased PI3K, AKT and p-AKT expression levels. Simultaneously, Mo or/and Cd upregulated ASC, NLRP3, NEK7, Caspase-1, GSDMA, GSDME, IL-18 and IL-1β mRNA levels and Caspase-1 p20, NLRP3, ASC, GSDMD protein levels, increased the percentage of pyroptotic cells, LDH , NO , IL-18 and IL-1β releases as well as relative conductivity. Moreover, NLRP3 inhibitor MCC950 and ROS scavenger BHA could ameliorate the above changed factors induced by Mo and Cd co-exposure. Collectively, our results reveal that combination of Mo and Cd synergistically cause oxidative stress and trigger pyroptosis via ROS/PTEN/PI3K/AKT axis in duck tubular epithelial cells.
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ACS Infectious Diseases
·
2025
·
IF 3.8
Hengxiu Wang,Hongchen Wang,Yue Yang,Tianming Wang,Changzhong Wang,Daqiang Wu,Caixia Zheng,Wenfan Wei
Berberine (BER), a natural isoquinoline alkaloid, exhibits broad-spectrum antifungal activity, yet its mechanism against Aspergillus fumigatus─a leading cause of invasive fungal infections─remains poorly understood. Here, we aim to unveil the mechanism of BER against the pathogenicity of A. fumigatus through mitochondrial dynamics and related pathways. In vitro assays revealed that berberine treatment triggered mitochondrial fragmentation, resulting in reactive oxygen species (ROS) overaccumulation. Subsequent proteomic analyses identified Hog1-MAPK as the central signaling hub activated by ROS stress. Upon activation, Hog1 localizes to the nucleus. ROS scavenging (N-acetylcysteine (NAC) treatment) abolished BER’s antifungal effects, confirming the ROS-Hog1-cell cycle axis. Crucially, in a murine invasive aspergillosis model, BER reduced the fungal burden in lungs and improved survival rates. Thus, we demonstrate that berberine suppresses A. fumigatus growth by disrupting mitochondrial dynamics, elevating reactive ROS, and activating the Hog1-MAPK signaling cascade, ultimately inducing cell cycle arrest. Our findings unveil a previously unrecognized mechanism linking mitochondrial morphology dysregulation to cell cycle control in fungi and establish BER as a promising therapeutic agent targeting mitochondrial-ROS-Hog1 signaling in A. fumigatus infections.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Zhiqing Lin,Haoyue Deng,Shuang Wang,Zhanfeng Wang,Guang Yang,Keke Huang
Oxidative stress in the retina and dysregulation of iron homeostasis are established as central pathogenic mechanisms in dry age-related macular degeneration (dAMD). Nonetheless, effective clinical treatments to counteract retinal degeneration in this condition are still absent. Our research began with developing a single-cell transcriptome profile of retinal tissue subjected to sodium iodate (NaIO 3 )-induced oxidative injury. This analysis identified ferroptosis in photoreceptor cells as a key driver of disease advancement. Apoferritin (AFn) is a hollow, spherical protein nanocage formed by 24 self-assembled subunits, enabling supramolecular iron storage through ferroxidase-mediated mineralization while providing dynamic iron buffering and antioxidant protection in biological systems. We then engineered a biomimetic nanoparticle, AFn-MNP, by combining Afn with melanin nanoparticles (MNP). AFn-MNP displayed significant ferrous ion-chelating ability and antioxidant activity, effectively mitigating NaIO 3 -triggered photoreceptor ferroptosis in vitro and in vivo. Significantly, a single intravitreal injection of 10 μg AFn-MNP effectively counteracted visual impairment in NaIO 3 -induced dAMD model mice, reversed damage to photoreceptor synaptic terminals, and significantly alleviated photoreceptor degeneration and retinal oxidative injury.In summary, our results indicate that AFn-MNP holds significant promise as a novel therapy for dAMD and other retinal degenerative diseases linked to oxidative damage and impaired iron metabolism.
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Biomaterials Science
·
2020
·Vol. 8
·期 22
·6204-6211
·
IF 6.183
Tao Wen,Aiyun Yang,Tao Wang,Mengfan Jia,Xinning Lai,Jie Meng,Jian Liu,Bing Han,Haiyan Xu
Chronic myeloid leukemia (CML) is a kind of hematological malignancy featured with retarded differentiation that is highly linked to the level of intracellular reactive oxygen species (ROS). In this work, ultra-small platinum nanoparticles deposited on gold nanorods (Au@Pt) were synthesized and applied on the CML cells. It was shown that Au@Pt had multienzyme-like activities that induced a fluctuation of the intracellular ROS level over the incubation time, depending on their temporal locations in the cells. The ROS fluctuation triggered cellular autophagy and enhanced the level of autophagic protein Beclin-1, which caused the degradation of fusion protein BCR-ABL, the key factor of retarded differentiation and led to the downregulation of phosphorylation of PI3K and AKT. These interactions together broke retarded differentiation and drove the CML cells to differentiate towards megakaryocytes, which is of great significance in enhancing leukemic cell apoptosis. Therefore, Au@Pt exhibited a novel function and promising therapeutic potential for the CML treatment.
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