INORGANIC CHEMISTRY
·
2025
·
IF 4.7
Qitao Wu,Zhenzhen Lin,Yuzhi Zou,Wenxin Huang,Yanshi Li,Xiaosen Huang,Jiankai Wang,Javokhir Toshov,Sardor Donaev,Hengcong Tao,Shunli Li
Electrocatalytic oxidation of 5-hydroxymethylfurfural to prepare high-value-added chemicals is an effective solution for a sustainable alternative to fossil fuels. We report a novel one-step hydrothermal sulfurization strategy to construct hierarchical FeNi-S@NF nanoflower architectures comprising interconnected 2D nanosheets. This catalyst design synergistically integrates high conductivity (i.e., nickel foam (NF) substrate), abundant active sites (i.e., 2D nanosheet), and optimized electronic structure (i.e., sulfur doping), achieving exceptional electrocatalytic 5-hydroxymethylfurfural (HMF) to 2,5-furandicarboxylic acid (FDCA) conversion. By optimizing the classical two-step hydrothermal sulfidation approach through precise control of metal ratios and sulfidation duration, we significantly enhanced the catalytic performance for the HMF oxidation reaction (HMFOR). Sulfur doping was found to substantially improve the catalyst’s adsorption capability for HMFOR intermediates, thereby enhancing both activity and selectivity toward FDCA production. The optimized FeNi-S@NF nanoflower catalyst demonstrated superior electrocatalytic performance in 1 M KOH + 50 mM HMF, achieving 98.41% conversion rate, 92.08% FDCA yield, and 89.19% Faradaic efficiency at an applied potential of 1.45 V vs a reversible hydrogen electrode (RHE), surpassing most reported transition metal-based electrocatalysts. This research work provides a new strategy for the rapid and low-cost synthesis of two-dimensional sulfide nanoelectrocatalysts for the efficient electrooxidation process of biomass derivatives.
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JOURNAL OF BIOMATERIALS SCIENCE-POLYMER EDITION
·
2024
·
IF 3.6
Shanjiang Chen,Jianjian Yang,Fuli Liu
Celastrol (CEL) belongs to the group of non-steroidal immunosuppressants with the potential to improve cardiac hypertrophy (CH). However, the poor biocompatibility and low bioavailability of CEL limit its in vivo application. This study was aimed to develop a targeted drug delivery system that can efficiently and safely deliver CEL to target tissues, providing a research basis for the application of CEL in CH therapy. A novel ROS-sensitive drug-loaded nanomicelle, dodecanoic acid (DA)-phenylboronic acid pinacol ester-dextran polymer encapsulating CEL (DBD@CEL), was synthesized using chemical synthesis. Then, the morphology, particle size, drug-loaded content, and ROS-responsive release behavior of DBD@CEL were studied. Pharmacokinetics and biocompatibility were evaluated using healthy mice. Finally, the ability and mechanism of DBD@CEL in improving CH in vivo were investigated using a mouse CH model. DBD@CEL was successfully prepared with a drug loading of 18.9%. It exhibited excellent stability with an average particle size of 110.0 ± 1.7 nm. Within 48 h, DBD@CEL released only 19.4% in the absence of H2O2, while in the presence of 1 mM H2O2, the release rate increased to 71.5%. Biocompatibility studies indicated that DBD@CEL did not cause blood cell hemolysis, had no impact on normal organs, and did not result in abnormal blood biochemical indicators, demonstrating excellent biocompatibility. In vivo studies revealed that DBD@CEL regulated the activation of NF-κB signaling, inhibits pyroptosis and oxidative stress, and thereby ameliorates CH. The ROS-responsive DBD@CEL nanodrug delivery system enhances the therapeutic activity of CEL for CH, providing a promising drug delivery system for the clinical treatment of CH.
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Journal of Translational Medicine
·
2026
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IF 9.7
Gao Hengyuan,Lin Junqing,Chen Xiaobing,Su Yingshi,Huang Yibin,Zhang Yubo,Zhang Junchang,Xu Nan,Dai Xiaoyong
Background Inter-tumor heterogeneity poses significant challenges for precision therapy in thyroid cancer (TC). The conventional organoid models are limited by inefficiency and poor physiological relevance. Methods We developed droplet-engineered organoids (DEOs) using microfluidic 3D bioprinting to rapidly generate patient-derived TC models. These DEOs were characterized via histology, whole-exome and RNA sequencing, and utilized for drug sensitivity testing and metastasis modeling. Results DEOs were generated within 10 days, exhibiting superior uniformity (CV: 2.54%) and a high success rate (76%). They faithfully recapitulated the histopathological architecture, genomic landscape (92% driver gene concordance), and native immune microenvironment (CD3+/CD56+/CD68+/α-SMA+) of parental tumors. Drug screening revealed patient-specific heterogeneity, accurately mirroring clinical responses, including cisplatin sensitivity and anti-PD-1 resistance. We established a novel TC and lung organoids co-culture model, which could be used to study the TC lung metastasis. Crucially, transcriptomics identified stage-specific maturation driven by NF-κB signaling. Pharmacological inhibition of NF-κB synergistically enhanced the efficacy of dasatinib, anti-PD-1, and paclitaxel, with combination index (CI) values of 0.58, 0.45, and 0.80, respectively. Conclusions Our microfluidic platform enables rapid, high-fidelity modeling of TC, offering a scalable and physiologically relevant tool for mechanistic studies, drug screening, and personalized therapy prediction, with highly promising translational potential.
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TOXICOLOGY
·
2026
·
IF 5.2
Yu Zhang,Yu-Qi Hong,Yi Liu,Ye Yuan,Zi-Xuan Lu,Xiang Zhang,Ting-Ting Zhu
Indium tin oxide nanoparticles (ITO NPs) are widely used in optoelectronic industries, and increasing occupational exposure has raised concern about their pulmonary toxicity. Although ITO exposure has been associated with severe lung diseases, the mechanisms underlying epithelial injury remain unclear. Here, a simplified macrophage–epithelial cell model using RAW264.7 macrophages and BEAS-2B epithelial cells was established to investigate how macrophages modulate ITO NP-induced epithelial toxicity. Direct exposure to ITO NPs caused limited toxicity in BEAS-2B cells, whereas conditioned medium from ITO NP-exposed RAW264.7 cells was associated with reduced epithelial viability, increased LDH release, and EMT-like changes. Dissolved indium species alone did not fully account for the observed effects, whereas macrophage-derived oxidative stress and associated inflammatory responses appeared to contribute more substantially to the epithelial responses. Transcriptomic and biochemical analyses showed that ITO NPs induced oxidative stress and activated NF-κB signaling in macrophages. Inhibition of ROS or NF-κB attenuated macrophage-derived cytotoxicity and reduced EMT-like changes in epithelial cells. These findings support a role for macrophages as important regulators of ITO NP-induced epithelial injury and provide additional mechanistic insight into ITO-related pulmonary toxicity.
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ChemCatChem
·
2023
·Vol. 15
·期 5
·e202201469
·
IF 4.5
Zhe Jia,Jiayin Shang,Kaijing Xue,Xi Yang,Sumin Wang,Changhua Xu,Qiguan Wang
Graphical High OER/ORR performances : boosted oxygen reduction reaction (ORR) as well as optimized oxygen evolution reaction (OER) and high-activity zinc-air batteries (ZAB), from a nitrogen-doped carbon nanomaterial (NCM) inserted Ni−Co layered double hydroxide (NiCo-LDH) electrocatalyst on nickel foam are achieved. The super thin NCM prepared by calcination of self-assembled perylenetetracarboxylic dianhydride/dicyandiamide improves the conductivity, electroactive surface area of NiCo-LDH nanoplates. Herein, a high performance bifunctional catalyst was prepared by inserting N-doped nanomaterials into Ni−Co layered dihydroxides (NiCo-LDH) nanoplates for high performance zinc-air battery. By using self-assembly of perylenetetracarboxylic dianhydride and dicyandiamide in the hydrothermal condition, a nitrogen-containing super thin carbonaceous nanosheet is achieved after calcination. Then NCM inserted NiCo-LDH nanoplates attached to nickel foam (NiCo-LDH/NCM@NF) are synthesized by in-situ production of NiCo-LDH species on NCM wrapped NF. The specific NCM improves the conductivity, electroactive surface area and the ORR/OER bifunctional activity of NiCo-LDH nanoplates. In addition, benefited from the formed rich oxygen vacancies, NiCo-LDH/NCM@NF delivers the low OER overpotential (352 mV at 50 mA cm −2 ) and boosted ORR performance with a half-wave potential of 0.765 V vs RHE. As the air cathode, the fabricated ZAB devices show a satisfactory capacity of 685 mAh g −1 and the energy density of 158 mW cm −2 .
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RESEARCH IN VETERINARY SCIENCE
·
2023
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IF 2.4
Jirao Shen,Feng Yang,Guibo Wang,Xiaoqing Mou,Jinyu Li,Xuezhi Ding,Xurong Wang,Hongsheng Li
Staphylococcus haemolyticus ( S. haemolyticus ) is one of the most common coagulase-negative staphylococci (CoNS) isolates from bovine mastitis . Paeoniflorin (PF) shows anti-inflammatory effects on different inflammatory diseases in vitro studies and in vivo animal experiments. In this study, the viability of bovine mammary epithelial cells (bMECs) was detected by the cell counting kit-8 experiment. Subsequently, bMECs were induced with S. haemolyticus , and the induction dosage was determined. The expression of pro-inflammatory cytokines and toll-like receptor (TLR2) and nuclear factor kappa-B (NF-κB) signaling pathway-related genes were investigated by quantitative real-time PCR. The critical pathway proteins were detected by western blot . The results showed that the multiplicity of infection (MOI; the ratio of bacteria to bMECs) 5:1 of S. haemolyticus for 12 h could cause cellular inflammation, which was selected to establish the inflammatory model. Incubation with 50 μg/ml PF for 12 h was the best intervention condition for cells stimulated by S. hemolyticus . Quantitative real-time PCR and western blot analysis showed that PF inhibited the activation of TLR2 and NF-κB pathway-related genes and the expression of related proteins. Western blot results showed that PF suppressed the expression of NF-κB unit p65, NF-κB unit p50, and MyD88 in bMECs stimulated by S. haemolyticus . The inflammatory response pathway and molecular mechanism caused by S. haemolyticus on bMECs are related to TLR2-mediated NF-κB signaling pathways. The anti-inflammatory mechanism of PF may also be through this pathway. Therefore, PF is expected to develop potential drugs against CoNS-induced bovine mastitis.
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ACTA BIOCHIMICA POLONICA
·
2022
·Vol. 69
·期 2
·363-370
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IF 2.349
Jian-li Qiu,Yu-na Chai,Feng-yang Duan,Hui-juan Zhang,Xiao-yan Han,Ling-yan Chen,Fei Duan
Liver fibrosis is a global health problem caused by a number of diseases related to liver damage. 6-Shogaol is a biologically active substance derived from the rhizome of Zingiber officinale Roscoe with anti-tumor, anti-inflammatory, and antioxidant properties. To explore the effects of 6-Shogaol on liver fibrosis, we used a mouse model of the condition in which mice were injected intraperitoneally with carbon tetrachloride (CCl4) at a dose of 2 mL/kg three times per week for a period of 4 weeks. 6-Shogaol was administered orally at two different doses (5 mg/kg, 20 mg/kg) 30 min before CCl4 injection. CCl4 induced severe liver injury and fibrosis, as indicated by significant inflammatory cell infiltration, disordered liver structure, increased activities of aspartate aminotransferase and alanine aminotransferase (liver damage markers) in serum, elevated collagen deposition, and overexpressed alpha-smooth muscle actin (α-SMA, marker of hepatic stellate cells activation) in liver tissues, whereas 6-Shogaol administration rescued those alterations dose-dependently. We found that 6-Shogaol suppressed CCl4-induced inflammatory response by inhibiting macrophage recruitment, release of pro-inflammatory factors, and activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in liver tissues. Additionally, we demonstrated that 6-Shogaol blocked CCl4-induced activation of the nuclear factor-kappa B (NF-κB) pathway, which is a vital transcriptional regulator of the inflammatory response. Altogether, this study demonstrates that 6-Shogaol can prevent CCl4-induced liver fibrosis by suppressing inflammatory response through the NF-κB pathway and suggests that 6-Shogaol can be used for liver fibrosis prevention.
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Frontiers in Immunology
·
2022
·
IF 8.786
Huanhuan Xu,Titi Liu,Jin Li,Fei Chen,Jing Xu,Lihong Hu,Li Jiang,Zemin Xiang,Xuanjun Wang,Jun Sheng
Tumor necrosis factor (TNF)-stimulated nuclear factor-kappa B (NF-κB) signaling plays very crucial roles in cancer development and progression, and represents a potential target for drug discovery. Roburic acid is a newly discovered tetracyclic triterpene acid isolated from oak galls and exhibits anti-inflammatory activity. However, whether roburic acid exerts antitumor effects through inhibition of TNF-induced NF-κB signaling remains unknown. Here, we demonstrated that roburic acid bound directly to TNF with high affinity ( K D = 7.066 μM), blocked the interaction between TNF and its receptor (TNF-R1), and significantly inhibited TNF-induced NF-κB activation. Roburic acid exhibited antitumor activity in numerous cancer cells and could effectively induce G0/G1 cell cycle arrest and apoptosis in colorectal cancer cells. Importantly, roburic acid inhibited the TNF-induced phosphorylation of IKKα/β, IκBα, and p65, degradation of IκBα, nuclear translocation of p65, and NF-κB-target gene expression, including that of XIAP, Mcl-1, and Survivin, in colorectal cancer cells. Moreover, roburic acid suppressed tumor growth by blocking NF-κB signaling in a xenograft nude mouse model of colorectal cancer. Taken together, our findings showed that roburic acid directly binds to TNF with high affinity, thereby disrupting its interaction with TNF-R1 and leading to the inhibition of the NF-κB signaling pathway, both in vitro and in vivo . The results indicated that roburic acid is a novel TNF-targeting therapeutics agent in colorectal cancer as well as other cancer types.
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JOURNAL OF ALLOYS AND COMPOUNDS
·
2022
·
IF 6.371
Rui Yao,Leran Liu,Jinwei Wang,Yun Wu,Qiang Zhao,Jinping Li,Guang Liu
Electrochemical water splitting is a vital means of producing hydrogen in the future. However, the sluggish kinetics of the oxygen evolution reaction (OER) at the anode of the water electrolysis limits its efficiency. Moreover, high current density (≥500 mA/cm 2 ) hydrogen production that meets industrial requirements and remains relatively stability is the trend currently. Herein, we reported a three-dimensional porous nanosheets array electrocatalyst FeVO 4 /NF-a synthesized by electrochemical activation and hydrothermal method . The developed FeVO 4 /NF-a electrode represents excellent OER performance at high current densities, which allows a low overpotential of 376 mV to achieve 1000 mA/cm 2 and keeps its durability for 50 h. Structural characterizations and electrochemical analyses show that the NF surface was converted to the active phase NiOOH for OER during electrochemical activation. The introduction of Fe 3+ and V 3+ changes the electron distribution of elements on the catalyst surface and optimizes its intrinsic activity. Additionally, the three-dimensional network structure of FeVO 4 /NF-a facilitates the gas diffusion and the contact between the catalyst with the electrolyte. This work will provide new ideas for hydrogen production from water electrolysis toward high current density.
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BIOSENSORS & BIOELECTRONICS
·
2022
·
IF 12.545
Feng Qiu,Xiaoyan Gan,Jianglong Yao,Bingying Jiang,Ruo Yuan,Yun Xiang
Transcription factors (TFs) are key substances in regulating the transcription, replication and expression of genes, and the detection of TFs can provide valuable information to diagnose a variety of diseases. By integrating hybridization chain reaction (HCR)-activated Cas12a enzyme with bio-responsive DNA hydrogels, we propose a dual amplification and label-free homogeneous electrochemical detection method to realize sensitive nuclear factor-kappa B p50 (NF-κB p50) detection. The presence of the target molecules protects the DNA duplex probes from digesting by exonuclease III and initiates HCR to generate long double stranded DNAs that can activate the activity of RNA-guided Cas12a enzymes. The single-stranded region of the DNA linkers that crosslink the DNA hydrogels can be cleaved by the activated Cas12a to release a large number of electroactive substances embedded in the gels, which exhibit highly enhanced electrochemical signals for detecting target molecules at the detection limit of 54.1 fM. In addition, the successful interrogation of NF-κB p50 spiked into lysate of HeLa cells by such method is also verified. The established method thus shows new opportunities for sensitive and convenient monitoring of other transcription factors and biomarkers.
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Reproductive Biology
·
2022
·
IF 2.089
Jing Xia,Shujuan Wu,Gengxiang Wu,Jing Yang
It has been reported that oxidative stress and chronic inflammation may be involved in the pathogenesis of polycystic ovary syndrome (PCOS). 8-oxoguanine DNA glycosylase (OGG1) is the main glycosylase that catalyzes the excision of DNA oxidation products. In this study, we investigated the role and potential mechanisms of OGG1 in the development of PCOS. We first analyzed OGG1 levels in serum and follicular fluid (FF) of PCOS patients , and significantly elevated OGG1 levels were noted in PCOS patients. We similarly observed a significant upregulation of OGG1 expression levels in ovarian tissue of the dehydroepiandrosterone (DHEA)-induced PCOS rat model. In addition, increased apoptosis and increased production of reactive oxygen species (ROS) were observed after the addition of OGG1-specific inhibitor (TH5487) in human granulosa-like tumor cell line (KGN) cells following a concentration gradient, along with a significant decrease in mRNA levels of inflammatory factors such as CXCL2 , IL-6, MCP1, IL-1β, and IL-18. Significant decreases in protein phosphorylation levels of P65 and IκBα were also observed in cells. In addition, we found a significant positive correlation between OGG1 and IL-6 expression levels in human and DHEA-induced PCOS rat models. In conclusion, our results suggest that OGG1 might be involved in the pathogenesis of PCOS by regulating the secretion of IL-6 through NF-κB signaling pathway , and there might be a balance between the inhibition of oxidative stress and the promotion of chronic inflammation by OGG1 on KGN cells.
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CHEMICO-BIOLOGICAL INTERACTIONS
·
2022
·
IF 5.168
Jiwen Liu,Yuting Wu,Shuhui Liu,Zhangshan Gao,Wentao Fan,Chenchen Ding,Zhihui Tang,Shuo Zhang,Xizhi Shi,Lei Tan,Yan Luo,Suquan Song
The bromoacetic acid (BAA) is one of the most teratogenic and neurotoxic disinfection byproducts . Birds take environmental water as their habitat and are inevitably affected by BAA in the environment. However, the neurotoxicity caused by BAA in birds has not been reported and the mechanism remains unclear. In this study, we chose chickens as the avian model to explore the effects of different concentrations of BAA on the brain tissues. Here, we selected the 3 μg/L dose of BAA detected in Tai Lake basin as a reference, and designed 1-, 100-, and 1000-fold of the environmental exposure dose as the experimental doses to explore the neurotoxicity of BAA in birds. Results showed that BAA increased the number of pyknotic nuclear neurons, deformed vascular sheaths, and glial cells in the brain. BAA inhibited the activity of antioxidant enzymes and the expression of antioxidant genes. With the increase of BAA concentration, the oxidative stress-responsive transcription factor NF-κB was activated. Furthermore, BAA remarkably changed the expression of lipid metabolism related genes (i.e., acc , gpat , hmgr , pparα , cpt1 , and ampkα ). Importantly, BAA decreased the mRNA and protein expression levels of autophagy-related genes (i.e., atg5 , ulk1 , beclin1 , and lc3 ). Meantime, BAA increased the mRNA and protein levels of apoptotic and pro-apoptotic genes, such as p53 , bax , cytochrome c , caspase-9 , and caspase-3 . Overall, our study provided new insights into the potential neurotoxic effects of BAA in birds, which was important for the clinical monitoring and prevention of BAA.
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