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Journal of Materials Chemistry A · 2018 ·Vol. 6 ·期 37 ·18003-18009 · IF 9.931

A smart nano-V2O5/ODA-coated mesh for a co-responsive photo-induced wettability transition and ROS generation for in situ water purification

Ruixiang Qu,Weifeng Zhang,Xiangyu Li,Yanan Liu,Tzungyu Shih,Yen Wei,Lin Feng

A co-responsive material is successfully fabricated by coating nano-vanadium pentoxide/octadecylamine (nano-V2O5/ODA) onto a copper mesh via a hydrothermal reaction. “Co-response” means that a material can realize a multi-performance transition under one environmental stimulus. Nano-V2O5 provides the material with a photo-induced wettability transition and reactive oxygen species (ROS) generation properties, while ODA produces a superhydrophobic material in its initial state. As a result, this material can achieve a reversible superhydrophobic/superhydrophilic transition under 254 nm ultraviolet (UV) light. By combining the wettability transition with ROS generation properties, a smart mesh can realize in situ photo-controlled water purification, i.e., the controllable and simultaneous removal of the oil and soluble contaminants. An extra V2O5-coated mesh is used as an auxiliary mesh to improve the oil removal and ROS generation efficiencies. Moreover, the mesh exhibits satisfactory reusability and physical/chemical stability, which is more promising for practical applications such as remote controlled water purification, timed discharge of sewage and microfluidic valves.

CAS / MDL: 124-30-1
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY · 2025 · IF 6.1

Copper excess induces autophagy dysfunction and mitochondrial ROS-ferroptosis progression, inhibits cellular biosynthesis of milk protein and lipid in bovine mammary epithelial cells

Ya Ting Fan,Dong Qiao Peng,Jing Lin Shen,Jun Hao Cui,Xin Yue Yang,Jin Ge Zhang,Yong Cheng Jin

Excessive copper (Cu) has the potential risk to ecosystems and organism health, with its impact on dairy cow mammary glands being not well-defined. This study used a bovine mammary epithelial cell (MAC-T) model to explore how copper excess affects cellular oxidative stress, autophagy, ferroptosis, and protein and lipid biosynthesis in milk. Results showed the increased intracellular ROS, MDA, and CAT ( P  < 0.05), alongside decreased T-SOD and GSH in CuSO 4 -treated cells ( P  < 0.05). Transmission electron microscopy and Ad-mCherry-GFP-LC3B assays revealed significant autophagosome accumulation in CuSO 4 exposed cells ( P  < 0.05). Additionally, CuSO 4 exposure modulated autophagy markers, evidenced by upregulation of genes such as LC3, ATG5, JNK1, and Beclin1, and downregulation of genes such as ATG4B, and p62 ( P  < 0.05). CuSO 4 also led to notable mitochondrial changes, including size reduction, membrane rupture, and cristae loss, and reduced expression of the ferroptosis inhibitor GPX4 ( P  < 0.05). The expression of mTOR, HIF-1α and β-catenin signaling pathway were inhibited in differentiated MAC-T cells by CuSO 4 exposure ( P  < 0.05), activated autophagy through activation of the AMPK-mTOR pathway which in turn affected downstream levels of genes related to milk protein and lipid. In conclusion, excessive copper induces oxidative stress in MAC-T cells, promoting autophagy through JNK-Bcl2, Beclin1-Vps34 and AMPK-mTOR pathways, leading to cell ferroptosis, as well as inhibits the cellular biosynthesis of milk protein and lipid.

CAS / MDL: 7758-98-7
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FOOD CHEMISTRY · 2024 · IF 8.5

New findings on post-mortem chicken quality changes: The ROS-influenced MAPK-JNK signaling pathway affects chicken quality by regulating muscle cell apoptosis

Yunhao Ma,Xinran Dong,Ying Wang,Zhaoming Wang,Yong Xie,Wendi Zhang,Daodong Pan,Hui Zhou,Baocai Xu

Research conducted previously has demonstrated that apoptosis significantly influences the chicken quality. While ROS are acknowledged as significant activators of apoptosis, the precise mechanism by which they influence muscle cell apoptosis in the post-mortem remains unclear. In this study, chicken samples were treated with rosemarinic acid and H 2 O 2 to induce varying ROS levels, and the ROS-triggered apoptosis mechanism in chicken muscle cells in post-mortem was analyzed. The TUNEL results revealed that elevated ROS levels in chicken were associated with a greater degree of muscle cell apoptosis. Western-blot results suggested that sarcoplasmic ROS could initiate apoptosis through the mitochondrial pathway by activating the MAPK-JNK signaling pathway. Moreover, TEM and shear force results demonstrated that muscle cell apoptosis initiates myofiber fragmentation and structural damage to sarcomeres, ultimately reducing chicken tenderness. This study enhances our understanding of post-mortem muscle cell apoptosis, providing valuable insights for regulating chicken quality.

CAS / MDL: 7722-84-1
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CHEMICAL ENGINEERING JOURNAL · 2024 · IF 13.3

NIR sensitive ZnO QDs decorated MXene hydrogel promotes spinal cord repair via tunable controlled release of Zn2+ and regulating ROS microenvironment of mitochondrion

Zelin Sang,Zepeng Liang,Grace Xuelian Huang,Zhenhua Chen,Xiuli Ren,Xifan Mei

Spinal cord injury (SCI) is one of the most devastating acute diseases. Zn 2+ has been verified plays a crucial role in SCI repair, however, how to continuously release zinc ions at the lesion site is still a cutting-edge challenge. Therefore, it is urgent to design a novel nanoplatform for promoting SCI repair with multifunction of controlled release of Zn 2+ and regulating ROS microenvironment of mitochondrion. Herein, we propose a protocol of preparing NIR sensitive ZnO quantum dots (QDs) decorated MXene hydrogel for SCI repair. TEM and EDS mapping showed that the ZnO QDs were uniformly distributed on the Mxene nanosheets. Catalase (CAT) analysis showed that the ZnO-Ti 3 C 2 nano enzymes could effectively scavenge ROS. Molecular biology studies showed that ZnO-Ti 3 C 2 @H repaired mitochondrial function by scavenging ROS with a clearance rate of up to 80 %. Neuronal apoptosis was subsequently reduced, and nerves and blood vessels were regenerated. NIR irradiation warmed the injury site to 42.9 °C, which enabled rapid enrichment of Zn 2+ at the lesion site. Footprinting and pathology experiments have shown that it improves functional recovery after injury and results in near-normal BMS scores. These results suggest that this multifunctional type of material incorporating NIR controlled release of Zn 2+ provides a promising strategy for promoting SCI repair.

CAS / MDL: 10196-18-6
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Acta Biomaterialia · 2024 · IF 9.4

Acidic biofilm microenvironment-responsive ROS generation via a protein nanoassembly with hypoxia-relieving and GSH-depleting capabilities for efficient elimination of biofilm bacteria

Junqin Li,Mengya Sun,Xiaoxian Tang,Yuqian Liu,Chunlei Ou,Yuze Luo,Li Wang,Luo Hai,Le Deng,Dinggeng He

Reactive oxygen species (ROS) are widely considered to the effective therapeutics for fighting bacterial infections especially those associated with biofilm. However, biofilm microenvironments including hypoxia, limited H 2 O 2 , and high glutathione (GSH) level seriously limit the therapeutic efficacy of ROS-based strategies. Herein, we have developed an acidic biofilm microenvironment-responsive antibacterial nanoplatform consisting of copper-dopped bovine serum albumin (CBSA) loaded with copper peroxide (CuO 2 ) synthesized in situ and indocyanine green (ICG). The three-in-one nanotherapeutics (CuO 2 /ICG@CBSA) are capable of releasing Cu 2+ and H 2 O 2 in a slightly acidic environment, where Cu 2+ catalyzes the conversion of H 2 O 2 into hydroxyl radical (•OH) and consumes the highly expressed GSH to disrupt the redox homeostasis. With the assistance of an 808 nm laser, the loaded ICG not only triggers the production of singlet oxygen ( 1 O 2 ) by a photodynamic process, but also provides photonic hyperpyrexia that further promotes the Fenton-like reaction for enhancing •OH production and induces thermal decomposition of CuO 2 for the O 2 -self-supplying 1 O 2 generation. The CuO 2 /ICG@CBSA with laser irradiation demonstrates photothermal-augmented multi-mode synergistic bactericidal effect and is capable of inhibiting biofilm formation and eradicating the biofilm bacteria. Further in vivo experiments suggest that the CuO 2 /ICG@CBSA can effectively eliminate wound infections and accelerate wound healing. The proposed three-in-one nanotherapeutics with O 2 /H 2 O 2 -self-supplied ROS generating capability show great potential in treating biofilm-associated bacterial infections. Statement of Significance Here, we have developed an acidic biofilm microenvironment-responsive nanoplatform consisting of copper-dopped bovine serum albumin (CBSA) loaded with copper peroxide (CuO 2 ) synthesized in situ and indocyanine green (ICG). The nanotherapeutics (CuO 2 /ICG@CBSA) are capable of releasing Cu 2+ and H 2 O 2 in an acidic environment, where Cu 2+ catalyzes the conversion of H 2 O 2 into •OH and consumes the overexpressed GSH to improve oxidative stress. With the aid of an 808 nm laser, ICG provides photonic hyperpyrexia for enhancing •OH production, and triggers O 2 -self-supplying 1 O 2 generation. CuO 2 /ICG@CBSA with laser irradiation displays photothermal-augmented multi-mode antibacterial and antibiofilm effect. Further in vivo experiments prove that CuO 2 /ICG@CBSA effectively eliminates wound infection and accelerates wound healing. The proposed three-in-one nanotherapeutics show great potential in treating biofilm-associated bacterial infections.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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FEBS Open Bio · 2024 · IF 2.8

2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer

Linqian Chen,Meifeng Chen,Yan Xie,Yuyan Zhang,Shutian Mo,Yongfei He,Tianyi Liang,Yuan Liao,Renbin Huang,Guodong Huang,Chuangye Han,Thi Thai Hoa Pham

Several studies have suggested a potential antitumor effect of 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD). To further understand the mechanism of action of this compound, we investigated its effect on the phosphatidylinositol-3-kinase (PI3K)/serine–threonine kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. We show that DMDD application significantly inhibited the proliferation of breast cancer cell lines MDA-MB-231 and ER-α positive MCF-7. Furthermore, DMDD application resulted in increased intracellular reactive oxygen species (ROS) levels, apoptosis and autophagy, whereas it downregulated the expression of PI3K, Akt and mTOR mRNA and proteins, and increased the expression of LC3II/I and p62 proteins. In a mouse breast cancer xenograft model, DMDD inhibited tumor growth. Expression analyses suggest that ROS levels were higher in DMDD treated tumor tissues, whereas immunohistochemical analyses suggest that apoptotic cells were more prevalent in the DMDD treated group compared to the control group. Taken together, our results suggest that the molecular mechanism of action of DMDD may involve the enhancement of breast cancer autophagy through the PI3K/Akt/mTOR signaling pathway by mediating ROS expression.

CAS / MDL: 589-41-3 33069-62-4
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JOURNAL OF NANOBIOTECHNOLOGY · 2025 ·Vol. 23 ·期 1 ·1-19 · IF 12.6

Polydopamine-based nano-protectant for prolonged boar semen preservation by eliminating ROS and regulating protein phosphorylation via D2DR-mediated cAMP/PKA signaling pathway

Wang Lirui,Xiong Manyi,Zhang Jian,Li Sisi,Ma Sheng,Jiang Shengyao,Jiang Yanping,Li Xinhong

Introduction Preservation of porcine semen is essential for artificial insemination and genetic improvement in pig breeding programs. However, the overproduction of reactive oxygen species (ROS) and lower levels of protein phosphorylation emerge as two challenges during semen preservation. Inspired by the innate ligand-receptor binding biofunction of dopamine, herein, a dual-task nano-protectant that combines ROS-scavenging and protein phosphorylation-regulating properties via incorporating the natural antioxidant epigallocatechin gallate (EGCG) into polydopamine nanoparticles (EGCG@PDA NPs) was proposed to enhance the quality of pig semen during storage at 4 ℃. The results suggested that EGCG@PDA NPs significantly maintained sperm motility, acrosome integrity and mitochondrial membrane potential, extending semen storage time from 3 days to 10 days. Furthermore, EGCG@PDA NPs effectively scavenged excess ROS and inhibited ROS-mediated sperm apoptosis through the extracellular regulated protein kinases (ERK) signaling pathway. Intriguingly, EGCG@PDA NPs could degrade into ultrasmall particles (< 10 nm) in the semen or H 2 O 2 systems. These particles could target and activate the dopamine D2 receptor (D2DR) on membrane surface of sperm midpiece, thereby enhancing protein phosphorylation via the downstream cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signaling pathway, ultimately improving sperm motility parameters. This study presents a novel nano-strategy to boost the quality of pig semen, offering significant implications for the pig industry. Graphical

CAS / MDL: 62-31-7 989-51-5
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Redox Biology · 2025 · IF 11.9

Injectable ROS homeostasis protective hydrogel inhibiting microglial ferroptosis through the Nrf2/Slc7a11/Gpx4 to alleviate neuropathic pain and promote spinal cord injury repair

Lu Li,Yu Cao,Xiangsheng Zhang,Jiayi Guo,Ziqiang Lin,Pengyu Zhou,Chuyin Chen,Jiahao Chen,Yike Liu,Danzhi Luo,Jiurong Chen,Yingdong Deng,Peng Sun,Zhiwen Zeng,Jun Zhou

Spinal cord injury (SCI) induced neuropathic pain (NP) remains a major clinical challenge due to persistent neuroinflammation and oxidative stress. We developed an injectable methacrylated and thiolated gelatin hydrogel loaded with quercetin (MSQ) to synergistically scavenge reactive oxygen species (ROS) and inhibit microglial ferroptosis for NP alleviation and neural repair. The MSQ hydrogel exhibited rapid photocrosslinking, sustained quercetin release, and robust ROS scavenging via thiol groups and quercetin, maintaining intracellular redox homeostasis. MSQ attenuated LPS-induced ferroptosis in BV2 microglia by upregulating Nrf2 expression, promoting its nuclear translocation, and activating the Slc7a11/Gpx4 pathway, thereby reducing lipid peroxidation and inflammatory cytokine release. Network pharmacology and molecular dynamics simulations confirmed quercetin's high-affinity binding to Nrf2. In a murine SCI model, MSQ implantation significantly reduced lesion area, suppressed microglial ferroptosis, and decreased pro-inflammatory mediators (TNFα, IL-1β, IL-6), while enhancing neuronal survival (Nissl/NeuN + cells) and axonal regeneration (MAP2/5-HT + expression). Motor functional recovery assays revealed improved BMS scores, gait regularity, and mechanical/thermal pain thresholds in MSQ-treated mice. This study highlights MSQ hydrogel as a multifunctional therapeutic platform that targets ROS homeostasis and microglial ferroptosis via the Nrf2/Slc7a11/Gpx4 axis, offering a promising strategy for post-SCI NP management and neural regeneration.

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American Journal of Translational Research · 2017 · IF 2.829

NADPH oxidase 2 inhibitor diphenyleneiodonium enhances ROS-independent bacterial phagocytosis in murine macrophages via activation of the calcium-mediated p38 MAPK signaling pathway

Yuanfeng Zhu,Shijun Fan,Ning Wang,Xiaoli Chen,Yongjun Yang,Yongling Lu,Qian Chen,Jiang Zheng,Xin Liu

Activation of NADPH oxidase 2 (NOX2) triggers reactive oxygen species (ROS) generation, both of which are essential for robust microbial clearance by phagocytes. However, it is unknown whether inhibition of NOX2 activation or ROS generation affects cellular phagocytosis. Here, we found that the classic NOX2 inhibitor diphenyleneiodonium (DPI) induced uptake of E. coli by murine peritoneal macrophages through enhancing phagocytosis, and this effect was temperature-sensitive and attenuated by cytochalasin D as well as chemical inhibition of Syk and PLCγ, two downstream kinases involved in actin polymerization during phagocytosis. DPI also decreased the production of TNF-α and IL-6 resulting from E. coli stimulation. The DPI-induced enhancement of phagocytosis was independent of NOX2 inhibition or ROS generation but depended on increased intracellular calcium and activation of the p38 MAPK signaling pathway. Furthermore, DPI enhanced bacterial elimination and ameliorated inflammation in E. coli -infected mice, leading to improved survival. Our results demonstrate that DPI facilitates ROS-independent bacterial phagocytosis by macrophages through activation of calcium and p38 MAPK signaling pathways.

CAS / MDL: 22144-77-0
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CYTOTECHNOLOGY · 2025 ·Vol. 77 ·期 2 ·1-18 · IF 1.7

TGF-β1 induces ROS to activate ferroptosis via the ERK1/2-WISP1 pathway to promote the progression of renal tubular epithelial cell fibrosis

Zhou Yi,Luan Fengwu,Feng Xiaonan,Yu Min,Li Lu,Guo Xiaoyan,Yin Xiaolong

Chronic kidney disease (CKD) often progresses to renal fibrosis, which is characterized by excessive extracellular matrix deposition and is also linked to ferroptosis. The present study investigated how TGF-β1 induces ferroptosis and thereby contributes to renal tubular epithelial cell fibrosis. Bioinformatics was employed to identify the differentially expressed genes relevant to renal fibrosis. An in vitro TGF-β1-induced fibrosis model of HK-2 cells was established, and the cell shape index was calculated. Fer-1, NAC, and PD98059 were utilized for targeted intervention, and their mechanisms were verified by transducing cells with WISP1-targeting shRNA lentivirus. Cell morphology was examined under a microscope, and cells were collected to determine the levels of ferroptosis-related factors (Fe 2+ , MDA, GSH, and LPO). Western blotting was performed to measure the levels of ERK1/2, WISP1, and ferroptosis indicators (GPX4 and hyperoxidized PRDX4). Flow cytometry was performed to determine the ROS levels and the rate of cell ferroptosis. TGF-β1 induced the transformation of HK-2 cells into fibroblast-like cells, leading to increased ROS levels, activation of the ERK1/2-WISP1 signaling pathway, and upregulation of ferroptosis and fibrosis-related factors. However, these effects could be effectively inhibited through pretreatment with Fer-1, NAC, and PD98059 individually, which further validated the involvement of the ERK1/2-WISP1 signaling pathway. In addition, WISP1 knockdown suppressed the cell transformation into fibroblast-like cells as well as the ferroptosis process, thereby reducing the expression levels of ferroptosis and fibrosis-related factors. The present study substantiated the process through which TGF-β1 elicits the production of ROS and triggers ferroptosis via the ERK1/2-WISP1 signaling pathway to facilitate the development of renal tubular epithelial cell fibrosis.

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Antioxidants · 2021 ·Vol. 10 ·期 7 ·1089 · IF 6.313

Seed Priming with Brassinosteroids Alleviates Chromium Stress in Rice Cultivars via Improving ROS Metabolism and Antioxidant Defense Response at Biochemical and Molecular Levels

Farwa Basit,Min Chen,Temoor Ahmed,Muhammad Shahid,Muhammad Noman,Jiaxin Liu,Jianyu An,Abeer Hashem,Al-Bandari Fahad Al-Arjani,Abdulaziz A. Alqarawi,Mashail Fahad S. Alsayed,Elsayed Fathi Abd_Allah,Jin Hu,Yajing Guan

This research was performed to explore the vital role of seed priming with a 0.01 µM concentration of brassinosteroids (EBL) to alleviate the adverse effects of Cr (100 µM) in two different rice cultivars. Seed priming with EBL significantly enhanced the germination attributes (germination percentage, germination energy, germination index, and vigor index, etc.), photosynthetic rate as well as plant growth (shoot and root length including the fresh and dry weight) under Cr toxicity as compared to the plants primed with water. Cr toxicity induced antioxidant enzyme activities (SOD, POD, CAT, and APX) and ROS level (MDA and H2O2contents) in both rice cultivars; however, a larger increment was observed in YLY-689 (tolerant) than CY-927 (sensitive) cultivar. EBL application stimulatingly increased antioxidant enzyme activities to scavenge ROS production under Cr stress. The gene expression of SOD and POD in EBL-primed rice plants followed a similar increasing trend as observed in the case of enzymatic activities of SOD and POD compared to water-primed rice plants. Simultaneously, Cr uptake was observed to be significantly higher in the water-primed control compared to plants primed with EBL. Moreover, Cr uptake was significant in YLY-689 compared to CY-927. In ultra-structure studies, it was observed that EBL priming relieved the rice plants from sub-cellular damage. Conclusively, our research indicated that seed priming with EBL could be adopted as a promising strategy to enhance rice growth by copping the venomous effect of Cr.Keywords:antioxidants;brassinosteroids;chromium;heavy metals;rice

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WATER RESEARCH · 2024 · IF 11.4

Combined exposure of emamectin benzoate and microplastics induces tight junction disorder, immune disorder and inflammation in carp midgut via lysosome/ROS/ferroptosis pathway

Xu Shi,Tong Xu,Meichen Gao,Yanju Bi,Jiaqi Wang,Yilin Yin,Shiwen Xu

Pesticides and plastics bring convenience to agriculture and life, but also bring residual pollution in the environment. Emamectin benzoate (EMB) is the most popular pesticide at present. The harm of microplastics (MPs) to water and aquatic organisms is gradually increasing, and the possibility that it appears synchronously with various pesticides increases. However, the damage of EMB and MPs to the carp midgut and its mechanism have not been clarified. Therefore, based on the EMB or/and MPs exposure models, this study explored the mechanism of midgut injury through transcriptomics, immunofluorescence, western blot methods, and so on. Studies in vivo and in vitro showed that EMB or MPs exposure caused cilia shortening, lysosome damage, and ROS overproduction, which led to Fe 2+ content increase, GSH/GSSG system disorder, lipid peroxidation, and ferroptosis. This process further led to the down-regulation of Cx43, Occludin, Claudin, and ZO-1, which further caused barrier damage, immune-related genes (immunoglobulin, IFN-γ) decrease and inflammation-related genes (TNF-α, IL-1β) increase. Combined exposure was more significant than that of single exposure, and the addition of EN6 and NAC proved that lysosome/ROS/ferroptosis regulated these midgut damages. In conclusion, EMB or/and MPs exposure induce tight junction disorder, immune disorder and inflammation in carp midgut through the lysosome/ROS/ferroptosis pathway.

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