INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.7
Yan-Ping Lin,Dong-Yan Zhou,Shang-Guang Du,Zi-Fan Yu,Rui-Na Zhou,Hao-Miao Li,Wei-Ming Chai
Protocatechualdehyde (PCA) is a better PPO inhibitor than ellagic acid. • PCA causes structural stretching and conformational change of PPO. • PCA is demonstrated as a potent anti-browning agent. • PCA regulates phenolic metabolism, reduces lipid peroxidation, boosts AsA-GSH cycle. • PCA regulates cell wall metabolism, inhibiting senescence-related browning. Polyphenol oxidase (PPO) is a vital polyphenol-metabolizing enzyme responsible for the enzymatic browning of fruits and vegetables. This study assessed the anti-PPO activity of protocatechualdehyde (PCA), yielding an IC 50 value of 94 μM (95% CI: 91.8 to 96.4 μM). Kinetic analysis revealed that PCA acted as a reversible and competitive inhibitor of PPO. Molecular docking indicated that hydrogen bonding and hydrophobic interactions were the main driving forces for PCA-PPO binding. Fluorescence spectroscopy further demonstrated that PCA binding altered the microenvironments around tyrosine and tryptophan residues, leading to conformational rearrangements and partial unfolding of the enzyme, evidenced by significant fluorescence quenching. Molecular dynamics simulation demonstrated that PCA perturbed the secondary structure of PPO and caused stretching of its overall structure, thereby inhibiting the catalytic activity of the enzyme. Furthermore, PCA demonstrated excellent anti-browning activity by regulating phenolic metabolism, reducing membrane lipid peroxidation, enhancing the ascorbic acid-glutathione cycle, and modulating cell wall metabolism to delay cellular senescence. Collectively, these findings offer some valuable insights into the development of PPO inhibitor and anti-browning agent, and provide a theoretical foundation for the potential application of PCA in the area of food preservation. Download: Download high-res image (249KB) Download: Download full-size image
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Discover Nano
·
2026
·Vol. 21
·期 1
·334
·
IF 6.7
Xuan Shaoyan,Yang Shenglei,Mao Yuqin,Chen Zhiyong,Zhu Yue,Zhou Ying,Huang Jie,Zhu Xiuliang,Wang Zuhua
Lung cancer remains one of the most prevalent and lethal malignancies worldwide. Oridonin (ORI) exhibits remarkable anti-lung cancer activity. Nevertheless, its clinical application in lung cancer therapy is severely hindered by poor solubility, fast metabolism, insufficient tumor penetration, and low selectivity. In this study, we developed a redox-responsive polymeric micelle (HA-cys-TOS) targeting the CD44 receptor to improve ORI bioavailability and tumor targeting. The polymer was synthesized via esterification and verified by 1 H NMR. Our data showed that ORI@HA-cys-TOS exhibited good stability, biosafety and redox-responsive sustained release. Compared to HepG2 cells, ORI@HA-cys-TOS exhibited significantly enhanced internalization ability in A549 cells, likely due to HA binding to the CD44 receptor overexpressed on A549 cells. Unexpectedly, the enhanced targeted accumulation of ORI@HA-cys-TOS micelles in vivo was also observed in both subcutaneous and in situ lung cancer tissues. In vivo and in vitro antitumor studies demonstrated that ORI@HA-cys-TOS micelles exhibited significantly greater antitumor activity compared to free ORI. Notably, no side-effects were observed during the 21 days experimental period. This study provides an experimental basis for advancing ORI toward clinical personalized lung cancer therapy by targeting CD44 and responding to the tumor redox microenvironment.
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CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Weiwei Zhang,Jiawen Shao,Xuanjun Zhang,Wanzhen Li,Longbao Zhu,Dongdong Sun,Lisandra L. Martin,Zuchun Zhao,Fei Ge
Glucose oxidase and CuS nanoparticles synergise with NIR photothermal therapy for antibacterial activity. • ROS-responsive GS 128 @HPQ hydrogel generates hydroxyl radicals to trigger controlled drug release. • GS 128 @HPQ hydrogel is self-healing, adhesive and mechanically stable for irregular wound treatment. • GS 128 @HPQ hydrogel accelerates diabetic infected wound healing with excellent biocompatibility. Diabetic chronic wounds are plagued by hyperglycemic microenvironments, multidrug-resistant (MDR) bacterial colonization and biofilm formation. In this study, glucose oxidase (GOx)/ 60 nm CuS nanoparticles were incorporated into an adhesive phenylboronic acid-modified, hyaluronic acid/quaternized chitosan (HA-PBA/QCS) dynamic boronate hydrogel (GS 128 @HPQ). GOx catalyzes glucose to generate H 2 O 2 , and CuS, under 808 nm near-infrared irradiation, acts as a Fenton-like catalyst to generate ·OH and also displays photothermal activity that elevates local temperatures to 45–65 °C in vitro, resulting in a synergistic antibacterial effect. The hydrogel has a porous structure with a pore size of approximately 50 μm, exhibits reactive oxygen species (ROS)-responsive drug release, possesses excellent mechanical properties including favorable rheological behavior, a tensile strength of 140 kPa, and self-healing capacity, and demonstrates adhesion properties ideal for wound dressing applications. In vitro, HA-PBA/QCS showed >98% MDR bacterial and more than 85% biofilm clearance. In diabetic mouse infected wound models, the wound area was <5% on Day21, with a > 70% downregulation of inflammation biomarkers IL-6/TNF-α and upregulation of VEGF/CD31, enables rapid re-epithelialization and collagen maturation, while the hydrogel has a hemolysis rate of less than 5%. This hydrogel provides a safe, efficient, and multifunctional platform for treating chronically infected diabetic wounds. Schematic diagram illustrating the synthesis pathway of the GS 128 @HPQ hydrogel and its application in diabetic wound repair through a combined chemo-photothermal antibacterial strategy. (Created in BioGDP). Download: Download high-res image (169KB) Download: Download full-size image
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ANALYTICAL CHEMISTRY
·
2026
·Vol. 98
·期 29
·21624-21633
·
IF 7.3
Zong Ziang,Qu Chaomin,Ding Leping,Ma Xiao,Abulipizi Gulizhabaier,Fang Yanlun,Li Li,Xie Wei,Wang Jiajia,Zhou Juanjuan,Li Zhanjun
Chemi-
or bioluminescence assays have broad applications
in biomedical
analysis, yet they still suffer from a flash effect or difficulty
in maintaining time synchronization during high-throughput assays.
Persistent luminescence (PersL) nanoprobes are able to emit photons
for a rather long time without any chemical reactions and have promising
applications in developing a physi-luminescence assay. Herein, SiO 2 /Zn 2 SiO 4 :Mn,Yb,Ge nanoparticles (MYG,
Zn/Si/Mn/Yb/Ge molar ratio, 2/15/0.003/0.060/0.100) were synthesized
with PersL properties at 525 nm. Mesoporous silica nanoparticles were
used as a nanotemplate to control the size and morphology, which allowed
for gram-scale production (1.1277 g). Ge was found to be an efficient
codopant to realize the enhanced PersL of MYG. A hydrophobic azo dye,
Sudan III, was loaded onto the MYG surface to form a quenched MYG-S
nanoprobe. Under 254 nm UV illumination, Sudan III was oxidized by
H 2 O 2 , and PersL was recovered. The “OFF–ON”
PersL property of MYG-S was applied to develop a physi-luminescence
assay method for H 2 O 2 , glucose, and glucose
oxidase in serum. As the PersL of the samples in a 96-well plate was
activated by simultaneous UV illumination rather than by adding chemicals,
high-throughput photographic luminescence analysis was realized with
accuracy and repeatability. Our research indicates the promising applications
of PersL nanoprobes in developing a physi-luminescence assay.
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MOLECULAR PHARMACEUTICS
·
2026
·Vol. 23
·期 8
·4341-4359
·
IF 4.9
Zhang Jieke,Li Yafang,Tian Chaoying,Zhang Xiaodi,Guo Jialing,Liu Chenxin,Wu Ligang,Du Bin,Cheng Genyang
Acute kidney injury (AKI) is a clinical syndrome with
high incidence
and mortality involving oxidative stress, ferroptosis, and inflammation,
yet there are no clinically effective interventions. Herein, HA@PDA@EGCG
nanoparticles were constructed using polydopamine (PDA) as carriers,
loaded with epigallocatechin gallate (EGCG) via π-π stacking,
and further surface-modified with hyaluronic acid (HA) through electrostatic
interaction. The nanoparticles had uniform morphology with a size
of approximately 50 nm and an EGCG loading capacity of 15.4 ±
0.8%. They exhibited prominent broad-spectrum antioxidant activity
and hydrogen peroxide-responsive EGCG release, with a cumulative release
rate of 58.2 ± 2.2% within 2 h and close to 80% at 12 h. Cellular
uptake and in vivo distribution confirmed the efficient CD44 receptor-mediated
internalization of the nanoparticles by human kidney-2 (HK-2) cells
as well as renal-targeted accumulation. Reactive oxygen species (ROS)
staining, mitochondrial morphology and apoptosis assays showed that
the nanoparticles effectively scavenged ROS, alleviated mitochondrial
damage, and inhibited cell apoptosis. In a cisplatin-induced in vivo
AKI model, HA@PDA@EGCG significantly restored renal function: blood
urea nitrogen and creatinine decreased to 12.3% and 27.2% of model
group levels, respectively, while alleviating renal pathological damage
and inflammation. Mechanistically, HA@PDA@EGCG inhibited ferroptosis
by downregulating acyl-CoA synthetase long-chain family member 4 (ACSL4)
to suppress lipid synthesis, chelating ferrous ions, and stabilizing
glutathione peroxidase 4 (GPX4) protein. Collectively, HA@PDA@EGCG
achieved renal protection by ameliorating oxidative stress, suppressing
inflammation and inhibiting ferroptosis through multiple pathways,
offering a novel strategy for targeted AKI therapy.
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Cell Reports
·
2026
·Vol. 45
·期 7
·
IF 7.7
Xiangyu Zhao,Tao Wu,Sanan Wu,Yujin Chen,Yu Zhang,Jing Chen,Kaixuan Diao,Zaoke He,Jiawei Yan,Tianzhu Lu,Chao Xu,Lu Liu,Gaofeng Fan,Dongliang Xu,Xinxiang Li,Xiaopeng Xiong,Jianjun Cheng,Fang Bai,Xue-Song Liu
Hypoxia, a hallmark of solid tumors, drives malignant progression and represents a major therapeutic challenge. Metabolic reprogramming induced by hypoxia creates unique metabolic vulnerabilities that can be exploited therapeutically. Here, we systematically compared the metabolic network differences between hypoxic and normoxic cells, and developed DepFormer, a transformer-based deep learning model, to nominate hypoxia-dependent metabolic genes in tumor cells. Oxidative phosphorylation was identified as the most significantly hypoxia-dependent metabolic pathway, and FLAD1 was predicted to be one of the key hypoxia-dependent metabolic genes. FLAD1 locus is amplified, and FLAD1 expression is upregulated across various tumor types, especially in hypoxic tumors. FLAD1 depletion disrupts activity of mitochondrial complex II, causing succinate/fumarate imbalance, which in turn prevents cancer cells from adapting to hypoxia. We further identified a drug-like inhibitor of FLAD1, which selectively inhibits growth of hypoxic tumor cells. Our study establishes DepFormer as an effective framework for predicting state-specific metabolic dependencies and reveals FLAD1 as a metabolic vulnerability and an innovative therapeutic target for hypoxic tumors.
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Asian Journal of Pharmaceutical Sciences
·
2026
·
IF 12.6
Xianbin Sun,Xinyi Wang,Fangying Zheng,Ruofei Xu,Xinyi Shen,Ding Tan,Xudong Li,Ya Wang,Kaiming Peng,Haijun Chen,Xiumei Li,Yu Gao
The rising threat of antibiotic resistance severely compromises the treatment of bacterial pneumonia, underscoring the urgent need for innovative and comprehensive therapeutic strategies. Here, we developed an innovative theranostic nanoplatform (Dex/BTGd) through the coordinated assembly of tetracycline, gadolinium ion (Gd 3+ ) and baicalin (Ba), which acts synergistically to combat infection, enable non-invasive magnetic resonance imaging (MRI), and regulate the lung microenvironment. Dex/BTGd demonstrated potent antibacterial activity against clinically relevant pathogens, effectively disrupting biofilms and overcoming tetracycline resistance. The incorporated Gd 3+ allowed targeted visualization of pulmonary infection sites by MRI, facilitating timely disease assessment. Beyond its direct antibacterial effects, the nanoplatform modulated the inflammatory microenvironment by scavenging reactive oxygen species, promoting macrophage polarization from the pro-inflammatory to the anti-inflammatory phenotype, and suppressing profibrotic transforming growth factor-β signaling. In a murine model of tetracycline-resistant Pseudomonas aeruginosa pneumonia, Dex/BTGd significantly reduced bacterial load, alleviated pulmonary edema and fibrosis, and enabled targeted MRI visualization of infected lesions. This integrated strategy of pathogen clearance, microenvironment modulation, and tissue repair offers a multifaceted solution to drug-resistant bacterial pneumonia, providing a promising blueprint for next-generation anti-infective systems.
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高影响因子
PEST MANAGEMENT SCIENCE
·
2026
·
IF 4.2
Hanchen Wei,Rui Xie,Shaoxiong Zhu,Feihu Bi,Linna Pan,Qiao Ye,Dalong Ren,Qingqing Wang,Yulong Wang,Bo Huang,Guang Yang
BACKGROUND Fungal diseases caused by Colletotrichum spp . severely threaten global agricultural productivity. Silver nanoparticles (AgNPs) offer potent antifungal activity, but their practical use is limited by instability, aggregation, and potential toxicity. This study aims to develop a safe, stable, and highly effective antifungal agent of carbohydrate-derived positively-charged glycopolymer-stabilized AgNPs (PGM@AgNPs) nanocomposites. RESULTS PGM@AgNPs exhibited an exceptionally narrow size distribution (7.41 ± 4.27 nm). The nanocomposite with the highest positive charge density ( m/n = 2:1) achieved almost 100% inhibition of Colletotrichum fructicola spore germination at 8 μg mL −1 , significantly outperforming naked AgNPs in inhibiting mycelial growth and cicada wing penetration. On pears, mangoes, and kiwifruits, PGM@AgNPs reduced anthracnose lesion sizes by 46–70%. Transcriptomic analysis revealed that the antifungal mechanism involves inducing oxidative stress, disrupting cellular integrity, and triggering autophagic cell death. Moreover, PGM@AgNPs showed negligible hemolysis and low cytotoxicity toward L929 cells and zebrafish. CONCLUSION The carbohydrate-derived PGM@AgNPs combine superior stability, enhanced antifungal efficacy, and favorable preliminary biocompatibility. By effectively alleviating anthracnose symptoms in postharvest fruits, these nanocomposites represent a promising, environmentally friendly alternative to chemical pesticides for sustainable agricultural disease management. © 2026 Society of Chemical Industry.
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Acta Physiologica
·
2026
·Vol. 242
·期 10
·e70299
·
IF 5.7
Wan Yu,Yanteng Wang,Na Li,Difei Wang
Aim Skeletal muscle atrophy is tightly associated with maladaptive alterations in mitochondrial function and morphology. Itchy E3 ubiquitin-protein ligase (ITCH) modulates mitochondria, and thrombospondin 1 (THBS1) positively regulates muscle atrophy, but their roles in muscle atrophy are unclear. Methods A muscle atrophy model was established in C57BL/6 mice via daily intraperitoneal injection of dexamethasone (Dex, 20 mg/kg). ITCH overexpression in skeletal muscle was achieved by adeno-associated virus serotype 9 injection. C2C12 cells were treated with 50 μM Dex to mimic in vitro muscle atrophy. Skeletal muscle atrophy in mice was evaluated using hematoxylin–eosin staining and immunofluorescence staining. Mitochondrial damage was assessed via transmission electron microscopy, succinate dehydrogenase staining, and JC-1 staining. Immunoprecipitation-liquid chromatography/mass spectrometry, molecular docking, and co-immunoprecipitation were used to investigate the interaction between ITCH and THBS1. Phosphoproteomics analysis was performed to detect the THBS1 downstream proteins. Results Dex treatment downregulated ITCH expression in skeletal muscle. ITCH overexpression increased body weight, muscle mass, and muscle strength, downregulated the expression of atrophy-related genes (Atrogin-1, Mstn, MuRF-1), and promoted mitochondrial biogenesis. The results of the C2C12 cells were consistent with those obtained in vivo. Proteomic profiling and Co-IP confirmed ITCH–THBS1 interaction and subsequent THBS1 ubiquitination. THBS1 knockdown reduced the expression of Atrogin-1 and MuRF-1 and inhibited the phosphorylation of JUN and Map3k7, whereas THBS1 overexpression reversed the ITCH-mediated improvement in mitochondrial biogenesis. Conclusion ITCH enhances mitochondrial biogenesis and mitigates Dex-induced muscle atrophy by promoting the ubiquitin-dependent degradation of THBS1 and subsequent inhibition of downstream JUN/Map3k7 phosphorylation. Practitioner Points This study clarifies a novel regulatory mechanism of skeletal muscle atrophy, confirming that the E3 ubiquitin ligase ITCH plays a protective role in dexamethasone-induced muscle atrophy. THBS1 acts as a critical downstream effector of ITCH, promoting muscle atrophy via activation of the JUN/Map3k7 phosphorylation signaling pathway. Targeting ITCH-dependent THBS1 ubiquitination may represent a potential strategy to mitigate skeletal muscle loss.
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TALANTA
·
2026
·
IF 6.7
Xiao Ma,Junjie Wang,Xin Chen,Jingcheng Li,Jiaqi Xue,Yufan Hou,Shihao Zhao,Jingxiang Zhao,Xiaomi Meng,Huajun Chen,Fang Wang,Fangya Guo,Jian Sun,Dan Zhao
Oxidase-like nanozymes use dissolved O 2 as the terminal electron acceptor and do not require exogenous H 2 O 2 , offering methodological advantages; however, conventional “one-pot carbonization” often causes concurrent carbonization and active-site formation, making the coordination environment difficult to control. Here, a sequential “pre-coordinate-polymerize-pyrolyze” site-engineering route was developed. On carbon black, OPD-Fe 3+ pre-coordination and in situ oxidative polymerization were carried out, followed by thermal treatment and purification, by which Fe–N moieties were immobilized within the shell region of the material to afford highly dispersed Fe–N x moieties predominantly featuring Fe–N 4 -like coordination (Fe–N 4 @CB d ). Multiscale characterization (XRD/XPS/XANES/EXAFS) consistently showed that iron resided predominantly in a first coordination sphere dominated by Fe–N (coordination number CN ≈ 3.7; R ≈ 2.01 Å), with no resolvable Fe–Fe scattering and only minor, non-dominant Fe-containing phases. ROS-trapping and time-dependent EPR measurements further confirmed continuous O 2 activation with the generation of O 2 • - , •OH, and 1 O 2 in the Fe–N 4 @CB d /O 2 system. DFT calculations additionally supported Fe–N 4 -like Fe–N x sites as the most plausible dominant active structures for O 2 activation. Under a unified TMB/O 2 system, steady-state enzyme kinetics exhibited outstanding performance, with V max = 351 nmol L −1 s −1 and K m = 0.56 mM, which are competitive among reports using the same substrate/readout. An H 2 O 2 -free colorimetric platform for alkaline phosphatase (ALP) was constructed on this material, achieving a low limit of detection and good linearity; acceptable accuracy and precision were verified by standard additions in diluted serum. This sequential strategy predefines the Fe–N neighborhood and topology at the precursor stage, reduces uncertainty in site formation, and avoids metal-organic framework (MOF)/hard-template/ionic-liquid multi-step procedures, thereby providing a strong basis for reproducible Fe–N 4 -like/Fe–N x oxidase-like nanozyme preparation and streamlined, robust bioanalysis.
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Advanced Healthcare Materials
·
2026
·
IF 11
Zi Zhu,Dan Yang,Hao Sun,Nizhaoyue Wei,Zhenkun Fu,Jia Zhang,Zhangdi Yan,Piaoping Yang,He Ding,Lei Zhong
Tumor immunotherapy exerts transformative effects in cancer treatment by leveraging intrinsic immunity and acting broadly effective across cancers, while first-line chemotherapy plays a direct role by disrupting tumor DNA and reducing burden. However, the clinical utility of immunotherapy is notably constrained by the immunosuppressive tumor microenvironment (ITME), while chemotherapy suffers from intrinsic systemic toxicity and acquired resistance. Herein, multifunctional nanozymes on cerium oxide sacrificial templates were designed via precursor engineering, with zirconium introduced to leverage the Kirkendall effect, whereby differing migration rates of zirconium and cerium ions form hierarchical porous structures. Accordingly, such structural features facilitate efficient mass transfer, thereby notably enhancing their triple enzymatic activity. Hierarchical architectures, coupled with hyaluronic acid moieties, further enable high-capacity cisplatin loading and high-specificity tumor targeting, effectively addressing poor drug delivery and off-target issues. Moreover, ultrasound-amplified redox homeostasis modulation driven by the nanozymes’ enzymatic activity acts as a key regulator for disrupting tumor cell redox balance. Meanwhile, synergy between oxidative stress and cisplatin-induced DNA damage acts as a dual stimulus to intervene in tumor survival pathways, not only reversing ITME but also mitigating chemotherapy-associated limitations, thereby fostering concurrent tumor cell death and immunogenic cell death and consequently highlighting promising prospects for malignancy therapy.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.7
Yumei Hu,Yuhang Xu,Biyu He,Du Niu,Xuechun Yang,Jiaping Huang,Zhenzhen Xie,Panpan Shen,Xian Li,Maosen Bai,Ziwei Liu,Hao Li,Yunyun Yang,Jian-Wen Huang,Chun-Chi Chen,Rey-Ting Guo,Longhai Dai
Ochratoxin A (OTA) is a pervasive and significant mycotoxin that poses serious health risks to humans and animals. The development of efficient biocatalysts for the enzymatic detoxification of OTA is of great importance. In this study, we enhanced the OTA-degrading activity of three amidohydrolases (ADHs) by up to ninefold. This improvement was achieved by reducing steric hindrance in the binding pocket and fine-tuning the hydrophilic interactions between the enzyme and substrate. The most efficient variant, Pw ADH/DM, was immobilized onto magnetic Fe 3 O 4 nanoparticles functionalized by the co -deposition of dopamine and polyethyleneimine. Under optimal conditions, this immobilization process achieved a high immobilization efficiency (85.4%) and activity recovery (76.9%). The immobilized enzyme exhibited enhanced pH stability and thermostability, along with good storage stability, reusability, and recyclability. More importantly, the immobilized enzyme completely degraded 100 ng/mL OTA in contaminated milk without affecting the milk's properties. These findings expand our understanding of the molecular mechanisms governing substrate binding and catalysis in OTA-degrading ADHs. Furthermore, they provide a blueprint for enzyme-based OTA decontamination during food processing.
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危险品化学品经营许可证（带存储）