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BIOLOGICAL TRACE ELEMENT RESEARCH · 2026 · IF 4.3

Fresh Dendrobium Officinale Polysaccharides Combine with Penicillamine to Attenuate Copper Overload-Induced Liver Injury in a Rat Model of Wilson’s Disease Via Activation of the Nrf2/HO-1/Keap1 Signaling Pathway

Zhang Shenao,Liu Pangwei,Jiang Yuge,Wu Huan,Cao Shijian,Xuan Shujuan,Wu Hongfei,Zhou An

Wilson’s disease (WD) is characterized by pathological copper accumulation, which drives hepatocellular oxidative stress and subsequent liver injury. While the first-line chelator penicillamine (PCA) effectively eliminates copper, it is associated with significant side effects. Dendrobium officinale polysaccharides, the active components in Dendrobium officinale , exhibit significant antioxidant and hepatoprotective effects. However, their potential in ameliorating liver injury in WD and as an adjunctive therapy to PCA remains unclear. This study investigated the hepatoprotective effects and underlying mechanisms of fresh Dendrobium officinale polysaccharides (FDOP), both alone and combined with PCA, in a copper-overloaded rat model. The results showed that FDOP significantly mitigated hepatic histopathological damage and reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (AKP). It also alleviated oxidative stress by decreasing hepatic malondialdehyde (MDA) and oxidized glutathione (GSSG) levels while enhancing superoxide dismutase (SOD) activity. Furthermore, FDOP promoted copper excretion and reduced copper deposition in the liver, brain, and kidneys. Mechanistically, FDOP activated the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway, evidenced by upregulated nuclear Nrf2 and HO-1 expression and downregulated Keap1 expression, thereby enhancing the cellular antioxidant defense system. Importantly, the combination of FDOP and PCA outperformed either monotherapy in alleviating liver injury, promoting copper excretion, and activating antioxidant pathways. In conclusion, FDOP not only exhibits excellent hepatoprotective effects but also holds potential as an adjunct to PCA therapy, offering a novel combined treatment strategy for WD.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF NANOBIOTECHNOLOGY · 2026 · IF 15

Glucose oxidase-mineralized scaffolds with multiple bioactivities for accelerated diabetic bone regeneration

Zhu Yancheng,Liu Xiaohao,Cai Zhuyun,Fan Yunshan,Zhou Zhi,Deng Guoli,Chen Feng,Li Shaohua,He Shisheng

Diabetic bone defects pose a significant clinical challenge due to impaired healing under hyperglycemia. However, no effective therapy is available to treat diabetic bone defect in clinic. This study engineers a biomimetic 3D-printed scaffold for diabetic bone regeneration by integrating glucose oxidase-mineralized amorphous calcium phosphate (GOx@ACP) nanoparticles into a gelatin methacryloyl (GelMA) hydrogel. Biomineralization encapsulates GOx within ACP, enhancing enzymatic stability and enabling glucose-responsive degradation. The scaffold exerts dual therapeutic actions consuming glucose to alleviate hyperglycemia while generating trace H₂O₂ to promote angiogenesis, alongside releasing osteogenic ions (Ca²⁺/PO₄³⁻) upon ACP degradation. The scaffold’s sustained degradation profile (with 61.02% mass retention after 28 days) ensures matched release kinetics of ions and enzymes, thereby synergistically promoting bone regeneration. In vitro, the scaffold significantly enhances bone marrow stromal cell proliferation, osteogenic differentiation with upregulated OPN/OCN/Runx2/Col-Ⅰ expression, and endothelial tubulogenesis. In diabetic rat cranial defects, the implantation significantly accelerated bone regeneration, with the bone volume (BV/TV) reaching approximately 52% by the 12th week. This enzyme-mineralized platform demonstrates promising potential for diabetic bone tissue engineering. Graphical

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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS · 2026 · IF 5.4

Synthesis of smart temperature responsive silicon quantum dots to stabilize Pickering emulsion for enhancing oil recovery

Zhe Wang,Han Jia,Xinbo Geng,Yang Liu,Zhihao Shen,Ruitong Xu,Yihan Huang,Debin Hou,Fujun Lu,Long Xu

The silicon quantum dots (SiQDs) exhibited application potential in enhancing oil recovery (EOR) owing to their ultrasmall size and extremely large specific surface area. In the present study, the temperature responsive silicon quantum dots (SiQDsP8400) were synthesized by grafting poly (ethylene glycol)-block-poly (propylene glycol)-block-poly (ethylene glycol) (PEG-PPG-PEG, average molecular weight was 8400) via facile and mild one-pot method, which were characterized by Fourier transform infrared spectrometer, X-ray photoelectron spectroscopy, dynamic light scattering and transmission electron microscopy. Their interfacial activity was systematically evaluated by interfacial tension, interfacial expansion modulus and water contact angle measurements. The SiQDsP8400 more effectively reduced the n-octane/water interfacial tension to 5.12 mN/m at 70 ℃, while that at 30 ℃ was 16.67 mN/m. The higher temperature weakened the hydrogen-bond interaction between grafted PEG-PPG-PEG and water molecule to promote the spontaneous migration of SiQDsP8400 to the interface. Then the stability and temperature response of SiQDsP8400 stabilized Pickering emulsion were evaluated. The EI value of emulsions was 86.58% at 70 ℃ after standing for 120 h, and then its sharp decrease in cooling process suggested their smart demulsification. Subsequently, the molecular dynamics (MD) was employed to confirmed the amphiphilicity changing of the PEG-PPG-PEG groups with increasing temperatures. Finally, the SiQDsP8400 stabilized emulsions enhanced oil recovery by 14.93% at 70 ℃ in core flooding experiment, and the produced emulsion conduct demulsification/re-emulsification cycles for 3 times by changing temperature. The study raised a novel design method for temperature responsive silicon quantum dots in EOR application.

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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES · 2026 · IF 8.7

Gallic acid-grafted chitosan and pullulan as a hydrogen bonding assembled, multifunctional coating for fruit preservation

Haihua Wang,Jianxia Yao,Ying Hou,Zhuoya Liu,Dong Yang

The development of eco-friendly and multifunctional edible coatings is crucial for mitigating postharvest losses of perishable fruits. Hence, a novel composite coating was engineered based on chitosan (CS) and pullulan (PUL) matrix, enhanced by a gallic acid-grafted chitosan (GS) conjugate synthesized through free radical grafting. The GS conjugate served as a multifunctional crosslinker, establishing a dense intermolecular network within the CS-PUL matrix primarily (CP) through hydrogen bonding, as confirmed by structural characterization. This molecular-level interaction significantly improved the mechanical strength (Tensile stress = 4.95 MPa, Elongation at break =121.21%) and barrier properties of the resulting coating. The chitosan/pullulan-gallic acid grafted chitosan (CP-GS) coating, applicable by spraying or dipping, exhibited remarkable antioxidant activity, achieving 97.8% DPPH radical scavenging (25 °C, 50% RH), the CP-GS coating significantly reduced weight loss, delayed the decline in titratable acidity, and effectively suppressed microbial growth, thereby extending the shelf life by 7 to 9 days compared to the uncoated samples. This study highlights the effectiveness of molecular grafting in designing advanced bio-based coatings and presents a promising strategy for fruit preservation using biological macromolecules.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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MICROCHEMICAL JOURNAL · 2026 · IF 5.2

Ultrasensitive detection of nanomolar valacyclovir based on MoS2/MWCNTs-COOH/GCE sensing platform

Na Liu,Youwei Jiang,Quanguo He,Tao Zhang,Yao Ping,Yelong Jiang,Wu Wang,Qijun Xie,Jianhua Ding

As an oral prodrug, valacyclovir undergoes rapid in vivo hydrolysis to form acyclovir - an agent with antiviral properties. This compound is extensively employed in addressing herpes virus infections and various other related conditions. Therefore, there is an urgent need to develop a method for detecting the content of valacyclovir in drugs. In this study, molybdenum disulfide (MoS 2 ) and carboxylated multi-walled carbon nanotubes (MWCNTs-COOH) were ultrasonically dispersed to prepare a suspension, which was drop-coated on the surface of a pretreated glassy carbon electrode (GCE). A MoS 2 /MWCNTs-COOH/GCE sensing platform was successfully constructed for the ultrasensitive detection of valacyclovir. Under optimized conditions, cyclic voltammetry (CV) was used to detect valacyclovir. A strong linear correlation between the oxidation peak current and the concentration was observed within the range of 0.1–40.0 μM, with a detection limit (LOD) of 0.013 μM. Meanwhile, the sensing platform also demonstrated excellent anti-interference capability, stability, and reproducibility. In the analysis of real samples, satisfactory recoveries for valacyclovir (96.5–104.0%) were achieved with a relative standard deviation (RSD) below 5.0%, further confirming its reliability. In summary, the developed MoS 2 /MWCNTs-COOH/GCE sensor offers a promising approach for the highly sensitive detection of valacyclovir.

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PROCESS SAFETY AND ENVIRONMENTAL PROTECTION · 2026 · IF 7.9

Synergistic Adsorption and Degradation of Tetracycline by Municipal Sludge-Based Biochar

Shiyuan Liu,Xueqiang Zhu,Damao Xu,Lai Zhou,Xiaoyi Li

Tetracycline (TC), a widespread aquatic contaminant, poses significant ecological risks. In this study, municipal sludge-based biochar (BC) was prepared by high-temperature pyrolysis to assess its efficiency and mechanism for TC removal. Various sources of BC exhibited effective TC removal, with BC pyrolyzed at 800 °C demonstrating the highest adsorption capacity at 173.42   mg/g (K800). Quenching and Electron Paramagnetic Resonance (EPR) analysis confirmed that persistent free radicals (PFRs) in BC facilitate the generation of superoxide radical (⸱O 2 - ) and singlet oxygen ( 1 O 2 ), promoting efficient oxidative degradation of TC. Brunauer-Emmett-Teller (BET), X-ray Photoelectron Spectroscopy (XPS), and Fourier Transform Infrared (FTIR) characterization identified the mesoporous structure, C-O, C=O groups, graphitic/pyridine nitrogen, and the Si-O-Si framework as key active sites. In summary, BC effectively removes TC through a synergistic process combining adsorption and degradation, offering a promising remediation strategy.

CAS / MDL: 3317-61-1 768-66-1
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CELLULAR AND MOLECULAR LIFE SCIENCES · 2026 ·Vol. 83 ·期 1 ·141 · IF 6.5

Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling: EVs promote VSMC phenotypic switching

Jia Wang,Xuan Shi,Di Wang,Jie Gao,Kangmo Huang,Juanji Li,Weichen Dong,Yunzi Li,Hongquan Guo,Yi Wang,Zhenqian Huang,Zhihui Liu,Li Huang,Liangyuan Pan,Xinfeng Liu,Wusheng Zhu,Mengna Peng,Gelin Xu

Background Despite the use of lipid-lowering and anti-inflammatory treatments, the progression of atherosclerosis is relentless in most patients. This suggests the presence of in situ pathological factors that continuously exacerbate lesions. We hypothesized that extracellular vesicles (EVs) within the atherosclerotic microenvironment might act as in situ stimulatory factors on vascular smooth muscle cells (VSMCs), thereby exacerbating atherosclerosis. Methods and results A local atherosclerosis model was induced using Ldlr knockout ( Ldlr KO) rats fed a high-cholesterol diet and subjected to partial carotid ligation. Immunofluorescence, Western blot (WB), and single-cell sequencing confirmed the phenotypic switching of VSMCs in atherosclerotic plaques from both rats and humans. The phenotypic switching of VSMCs in atherosclerotic rats was characterized by reduced expression of VSMC contraction markers and increased expression of LGALS3, PDGFRB, and SCA1. GW4869 inhibited the phenotypic switching of VSMCs in atherosclerotic plaques in a rat model. EVs were extracted from atherosclerotic carotid tissues using differential centrifugation. Chitosan thermosensitive hydrogels were used for in situ delivery of EVs into the arterial wall of the carotid artery. Immunofluorescence staining revealed that atherosclerotic plaque-derived EVs (AS-EVs) promoted VSMC phenotypic switching and downregulated the expression of VSMC contractile markers in vitro. miRNA analysis of EVs derived from atherosclerotic plaques of rats identified miR-23a-3p and its target gene Myl12b . To investigate the underlying mechanisms, engineered EVs loaded with miR-23a-3p were used to mimic AS-EVs. AS-EVs potentially regulate MRTFA nuclear translocation via miR-23a-3p/ Myl12b , inhibit contractile marker expression, promote VSMC phenotypic switching, and further promote carotid artery remodelling. Conclusion We conclude that AS-EVs promote VSMC phenotypic switching and exacerbate atherosclerosis. Supplementary Information The online version contains supplementary material available at 10.1007/s00018-026-06094-4.

CAS / MDL: 13408-09-8 9012-76-4
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FOOD CHEMISTRY · 2026 · IF 10.4

Myricetin-loaded ethyl cellulose/carboxymethyl cellulose nanoparticles to inhibit the formation of parent and oxygenated polycyclic aromatic hydrocarbons in baking systems

Xin Ma,Shimin Wu

Parent and oxygenated polycyclic aromatic hydrocarbons (PAHs and OPAHs) pose a threat to public health; however, few studies have reported strategies to mitigate their formation during baking, particularly for OPAHs. This study aimed to inhibit the formation of PAHs and OPAHs in baking systems using myricetin (Myr)-loaded ethyl cellulose (EC)/carboxymethyl cellulose (CMC) nanoparticles. The nanoparticles improved the water solubility and antioxidant activity of Myr. Molecular dynamics simulations revealed that the binding affinities followed the order: EC-Myr > CMC-Myr > EC-CMC. In baking systems, the nanoparticles effectively reduced the concentrations of 24 PAHs and 12 OPAHs, exhibiting stronger inhibitory effects than free myricetin. GC–MS/MS and electron paramagnetic resonance analyses revealed that CMC and Myr synergistically suppressed PAHs and OPAHs formation by reducing intermediates and unsaturated carbon-centered radicals. Overall, this study first provided a novel approach to reducing the concentrations of PAHs and OPAHs and their associated health risks in baking systems.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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CHEMICAL ENGINEERING JOURNAL · 2026 · IF 12.5

Triple-synergistic nanotherapeutics for acute and chronic colitis management via programmable multidimensional modulation

Penghui Wang,Yue Zhao,Ning Tian,Xiangling Liu,Tenghui Tian,Difu Zhu,Fangbing Liu,Hengyan Liu,Ling Li,Zhiyu Ren,Deok Chun Yang,Lei Zhao,Haijiao Xie,Rui Jiang,Yingnan Jiang

Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease characterized by persistent oxidative stress, dysregulated immunity, epithelial barrier disruption, and microbial imbalance, all of which synergistically exacerbate mucosal injury. Addressing these multifactorial challenges remains a critical obstacle in UC therapy. Here, we present a targeted ternary nano-therapeutic platform that integrates cobalt single-atom nanozymes (Co SA), ginsenoside Rb1 (Rb1), and Bifidobacterium bifidum (BB) for multidimensional intervention. Co SA exhibits enzyme-like catalytic activity to scavenge reactive oxygen species and mitigate oxidative stress. Rb1 suppresses pro-inflammatory signaling, promotes tight junction expression, and restores barrier integrity. Meanwhile, BB colonizes the inflamed colon, modulates gut microbiota, and enhances metabolic recovery. Through this synergistic design, the ternary system effectively attenuates oxidative injury, alleviates inflammation, repairs barrier dysfunction, and rebalances the gut microenvironment. In both acute and chronic UC models, this strategy achieved markedly superior therapeutic outcomes compared to individual components or clinical positive controls. Collectively, this work demonstrates a cost-effective, multifunctional, and translatable therapeutic approach, offering a new paradigm for the clinical management of UC.

CAS / MDL: 30418-59-8 68-12-2
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Food Bioscience · 2026 · IF 6.2

Dual signal amplification-based lateral flow strip for rapid and sensitive detection of streptomycin in milk

Wanqi Zhang,Lu Han,Yanhao Yin,Yaoting Mou,Yuhang Tian,Zhicong Sun,Yanfang Wu,Dongfei Chen,Yemin Guo,Xia Sun,Falan Li

Excessive streptomycin (STR) residues pose significant risks to dairy product quality and safety. Thus, developing highly sensitive detection methods for STR is essential to safeguard dairy safety and public health. In this study, we present a dual signal amplification lateral flow strip (LFS) using enzyme-assisted cycling and composite probe composed of multiple gold nanoparticles (AuNPs) for STR detection. Through targeted mutation, an optimized aptamer (Apt52-0) with both high affinity for STR and recognition by nicking endonuclease was developed, exhibiting enhanced binding to STR with a K d value of 6.87 nM, compared to the original Apt52. Enzyme-assisted amplification was achieved using the hairpin structure of the Apt52-0, Vent (exo-) DNA polymerase, and Nt.Alwl nicking endonuclease, enabling dual cycling of the target and double-stranded DNA (dsDNA). The cyclic products were then isothermally amplified, and composite probe composed of multiple AuNPs was utilized to construct a dual signal amplification lateral chromatography sensor for STR detection. This aptamer-based LFS achieved a visual limit of detection (LOD) of 25 nM, and a LOD of 17.6 nM analyzed via ImageJ software. The test strip demonstrated promising sensing performance in practical application, with STR recovery rates of 95.8%–103.9% in milk samples. This dual signal amplification-based LFS offers an inexpensive, rapid and sensitive approach to STR detection.

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CHEMICO-BIOLOGICAL INTERACTIONS · 2026 · IF 5.2

Potent genotoxicity of phenytoin in adult male C57BL/6J mice, an effect requiring metabolic activation (possibly by Cyp2c enzymes)

Manxin Chen,Haiting Sun,Shunda Zhu,Hang Yu,Yungang Liu

Phenytoin is a long standing antiepileptic drug with confirmed teratogenicity and possible carcinogenicity. Phenytoin formed electrophilic metabolite and induced oxidative DNA damage in vitro , yet it was negative in genotoxicity assays in rodents following 1∼3 d exposure. We hypothesized that extended exposure durations from regular regimens may enhance its metabolic activation and genotoxicity. In this study, male C57BL/6J mice were administered with phenytoin by gastric gavage at 5∼20 mg/kg (b.w.)/d for 7 d (5 mice in each group), then a comet assay with isolated hepatocytes, a Western blot assay of hepatic γ-H2AX (indicating double-strand DNA breaks), and a micronucleus test in the bone marrow polychromatic erythrocytes were performed. Positive results were observed in the above genotoxicity assays with phenytoin at 10 and/or 20 mg/kg/d doses, evidencing its DNA-breaking and chromosome-damaging effect. The protein levels of hepatic Cyp2c38, Cyp2c39, Cyp3a11, pregnane X receptor (PXR) and constitutive androstane receptor (CAR) (both receptors transcriptionally regulating Cyp2c enzymes) were all increased in the 10 and/or 20 mg/kg/d phenytoin groups. Additionally, co-exposure of 1-aminobenzotriazole (100 mg/kg/d, a wide-spectrum Cyp inhibitor) blocked the genotoxic effects and phenytoin-induced Cyp2c38, 2c39 and CAR protein expression. In a mouse hepatocarcinoma (Hepa1-6) cell line, phenytoin alone induced micronucleus weakly, however, dexamethasone (DEX, 0.1 μM, a Cyp2c inducer) obviously potentiated the effect, which could be further blocked by sulfaphenazole (50 μM, a Cyp2c inhibitor). This study suggests that following 7-d oral administration phenytoin could be genotoxic in mice (potency being close to N -nitrosodiethylamine), which requires metabolic activation, possibly by Cyp2c enzymes.

CAS / MDL: 526-08-9 55-18-5 50-02-2
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Acta Pharmaceutica Sinica B · 2026 · IF 14.6

Dual-Mode hepatoprotective nanoplatform combines ROS scavenging and FGF21 activation for precision acute liver injury therapy

Xinyu Tan,Man Li,Zhibin Lan,Wenxiang Zhang,Junjie Zou,Yibo An,Jingwen Zheng,Xuwen Xiang,Jing Lin,Sheng Lin,Wenjie Ni,Lin Che,Gang Liu,Jing Chen,Zhixiang Lu

To address the intertwined pathologies of oxidative stress, immune dysregulation, and lipid metabolic disorders in acute liver injury (ALI), we engineered an innovative nanosystem: M2@SAM-F21. M2@SAM-F21 features an M2 macrophage membrane coating encapsulating diselenide-bridged mesoporous silica nanoparticles for silymarin and FGF21 plasmid DNA codelivery, enabling synergistic multidimensional treatment. First, reactive oxygen species (ROS)-responsive oxidative stress is mitigated. Diselenide bonds undergo ROS-triggered cleavage, achieving precise silymarin release that efficiently scavenges multiple ROS types, significantly mitigating hepatic oxidative damage. Simultaneously, FGF21 drives immune reprogramming. Efficiently expressed FGF21 protein drives macrophage polarization toward the M2 anti-inflammatory phenotype, effectively reducing proinflammatory cytokine levels, with TNF- α decreased to 61 pg/mL and IL-6 reduced to 20 pg/mL, while increasing IL-10 to 68 pg/mL to reverse the immune microenvironment imbalance. In addition, metabolic homeostasis is restored. Activated fatty acid oxidation pathways substantially decrease serum concentrations of total cholesterol (TC) to 4.984 mmol/L and triglycerides (TG) to 0.586 mmol/L, and almost reduce hepatocellular lipid droplet accumulation by 76%, resolving metabolic dysregulation. In both alcoholic and drug-induced ALI models, M2@SAM-F21 demonstrates exceptional hepatoprotection. For example, it significantly restores serum alanine aminotransferase (ALT) to 46.6 U/L and aminotransferase (AST) to 180 U/L in the alcoholic ALI model, while markedly alleviating histopathological vacuolization and steatosis, with biological distribution imaging confirming inflammation-targeted accumulation and proteomic analysis further elucidating therapeutic mechanisms. Exhibiting superior biosafety and dual therapeutic-prophylactic potential, this system serves as a pioneering paradigm that integrates targeted delivery, intelligent release, and multipathway synergy for ALI treatment.

CAS / MDL: 1898-66-4 7727-21-1
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