Food Bioscience
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2026
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IF 6.2
Haiwang Liu,Zhongyan Bao,Yu Gao,Fengqin Feng,Minjie Zhao,Qing Lv,Qian Yang,Xi Zhang
Drug-induced malnutrition resulting from long-term glucocorticoid therapy has increasingly become a clinical concern. Dietary-derived active peptides represent an effective nutritional intervention strategy, yet the specific mechanisms of action of albumin peptides (AP) remain unclear. This study systematically evaluated the therapeutic effects of AP in a Dexamethasone (DEX)-induced malnutrition mouse model and elucidated its mechanisms through integrated analyses of liver transcriptomics, non-targeted metabolomics, and quantitative fatty acid profiling. Results demonstrated that AP administration ameliorated DEX-induced protein catabolism, increased serum prealbumin (PAB) levels by 183.66%, elevated total protein (TP) levels by 14.6%, and significantly reversed hepatic steatosis and gastrocnemius muscle degeneration. Transcriptomic analysis revealed that peroxisome proliferator-activated receptor alpha (PPARα) was the primary signaling pathway affected by AP, with gene expression levels of Ppara and related genes restored to normal ranges. Non-targeted metabolomic analyses further identified correlations between this transcriptional response and prostaglandin, leukotriene, and diacylglycerol levels. Fatty acid quantification showed that AP restored hepatic arachidonic acid levels by 17.3%. Correlation analyses revealed a significant positive relationship between hepatic arachidonic acid levels and PPARα expression (R≥0.97), reinforcing the hypothesis that arachidonic acid serves as a key endogenous ligand mediating the interaction between AP and PPARα. Additionally, AP restored short-chain fatty acid concentrations in feces, indicating the pivotal role of the gut-liver axis in phenotypic development. Together, these findings suggest that AP alleviates DEX-induced malnutrition partly through restoration of hepatic arachidonic acid metabolism and reactivation of PPARα signaling, supporting its potential as a functional food ingredient for drug-induced malnutrition.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
·
IF 8.7
Limei Zhu,Rongrong Pan,Rongjiao Sun,Yueqi Jin,Kemin Yang,Xianzhu You,Jiante Li,Jiangqian Kong,Ying Tan,Jiajia Dong,Wanle Hu
Ulcerative colitis (UC) is a chronic inflammatory bowel disorder characterized by mucosal barrier disruption, dysregulated immune activation, and microbial dysbiosis. However, current therapies are limited by systemic toxicity, poor retention at inflamed sites, and insufficient promotion of mucosal healing. Here, we engineered an injectable and self-healing hydrogel via dynamic Schiff base cross-linking between carboxymethyl chitosan (CMCS) and dialdehyde starch (DAS), loaded with dexamethasone (DEX) for localized anti-inflammatory delivery. The resulting CMCS/DAS hydrogel exhibited excellent biocompatibility, robust tissue adhesion, and mechanical resilience, which are crucial for ensuring sustained DEX release and reliable retention in the dynamic colonic environment. In vitro , the hydrogel demonstrated pronounced immunomodulatory efficacy through the promotion of macrophage polarization. In a TNBS-induced rat model of UC, the hydrogel treatment significantly attenuated inflammation, promoted epithelial integrity and barrier repair, and effectively rebalanced gut microbiota composition by enriching beneficial commensals. This multifunctional platform simultaneously addresses the central pathological processes of UC and provides a promising strategy for achieving durable therapeutic remission.
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Journal of the American Chemical Society
·
2026
·
IF 16.6
Zuoxi Zhang,Kexin Yin,Bowen Li,Huining He,Yang Bai,Bin Zheng
The cytoskeleton, an indispensable component during cell migration and proliferation, relies on the regionalized programming of intracellular proteins─liquid–liquid phase separation (LLPS) that enables cells to shift between phenotypes to determine their fate of migration and reproduction. However, the precise manipulation of the G/F-actin is extremely challenging, and effective direct regulatory measures are currently lacking to intervene in the physiological and pathological processes of cells. Herein, through LLPS visualization experiments, we reveal a storage and regulatory mechanism of cytoplasmic G-actin in cells via LLPS. Based on the conversion mechanism between stored G-actin and active G-actin within the free actin pool in the cytoplasm, G-actin’s LLPS forms droplets to participate in cellular activities. Furthermore, based on orthogonal disulfide chemistry reactions, we developed a cross-linker capable of altering the formation of actin bioaggregates. By screening targeted modification groups and backbone libraries, we designed the penicillamine-linked 4Arm-PEG (4Arm-Pen) capable of cross-linking with actin. Visualization of LLPS reversal intra- and extracellularly, 4Arm-Pen target proteomics, and mathematical modeling of F-actin polymerization kinetics collectively confirm that 4Arm-Pen not only cross-links G-actin, impeding droplet formation, but also influences the polymerization kinetics of F-actin, causing the cells to lose their invasive capacity. Furthermore, we demonstrated that G-actin depletion induced by cross-linking renders cancer cells immotile and triggers alterations in endogenous cellular mechanical parameters. Collectively, these findings provide deeper insights into the analysis and modulation of G-actin LLPS in cells, paving a path toward promising therapeutic strategies for cancer treatment.
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Acta Biomaterialia
·
2026
·
IF 10.4
Qiu-Shuang Cheng,Sheng-Chang Luo,Kai Fan,Zhi-Hong Chen,Jia-Xuan Yang,Jiu-Tao Cao,Bing-Bing Zheng,Zhi-Yuan Lan,Shi-Bin Wang,Pei-Yao Xu,Ai-Zheng Chen
The effective management of oral ulcers is hindered by the constantly moist oral environment and persistently dysregulated inflammatory microenvironment. Inspired by the hierarchical architecture of native mucosa, we engineered a biomimetic bilayer patch to achieve immune modulation and synergistic tissue regeneration. Compositionally mimicking the bioactive lamina propria, the patch features a bioadhesive inner layer enriched with dopamine-modified esophageal mucosa decellularized extracellular matrix (eECM-DA) to specifically recapitulate the native biochemical niche, embedded within hyaluronic acid methacrylate (HAMA) networks loaded with dexamethasone (Dex). Structurally mimicking the protective epithelial barrier, this inner matrix was coupled with a hydrophobic ethylcellulose (EC) backing to shield against saliva erosion. After contact with the moist oral environment, this eECM-DA/HAMA/EC-Dex (EDH/EC-Dex) bilayer patch rapidly contacts the wound and displaces interfacial water to achieve robust wet adhesion. Functionally, the EDH/EC-Dex patch actively reprogrammed the inflammatory milieu in lipopolysaccharide (LPS)-stimulated macrophages by modulating JAK-STAT signaling and antioxidant networks, thereby driving inflammation resolution and promoting orderly regulation of the ulcer microenvironment. In a rat oral ulcer model, EDH/EC-Dex patches demonstrated superior efficacy in accelerating re-epithelialization and functional recovery compared to commercial products. This work introduces an immune-modulatory, ECM-derived platform, offering a promising strategy for oral ulcer management and broader tissue engineering applications. Statement of significance A mucosa-inspired bilayer patch is developed for treating oral ulcers. This ECM-derived patch achieves robust wet adhesion and provides a protective barrier against saliva erosion through its bioadhesive inner layer and hydrophobic backing. Mechanistically, it actively regulates JAK-STAT signaling and antioxidant networks, effectively reprogramming the dysregulated inflammatory microenvironment to promote rapid re-epithelialization and functional recovery. This study offers a translatable biomaterial strategy for improving clinical management of oral ulcers. Download: Download high-res image (421KB) Download: Download full-size image
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Food Bioscience
·
2025
·
IF 5.9
Qianqian Wang,Juan Du,Enling Ye,Zhongyan Bao,Minjie Zhao,Jing Wang,Fengqin Feng,Weihong Min,Hong Yang
The goal of this study was designed to investigate the alleviating effects and mechanisms of wheat peptides (WP) on dexamethasone (DEX)-induced sarcopenia in mice. Furthermore, this study sought to validate the anti -sarcopenic efficacy of peptides identified through integrated in silico screening and peptidomic analysis in DEX-induced zebrafish model. The findings exhibited statistically significant enhancements in skeletal muscle strength (grip strength and swimming exhaustive time) and mass (gastrocnemius and soleus indexes) with oral administration of WP. In addition, metabolomics analysis identified N1-Methyl-2-Pyridone-5-Carboxamide and creatine are the crucial metabolites regulated by WP, associated with enhancements in muscle functionality in mice experiencing sarcopenia. WP counteract DEX-induced suppression of fibroblast growth factor receptor 1 (FGFR1) expression, subsequently regulated downstream mammalian target of rapamycin complex 1 (mTORC1) expression, thereby stimulating muscle protein synthesis and ameliorating sarcopenia in mice. Furthermore, docking analysis indicated that WP-derived peptides characterized by high abundance and favorable PeptideRanker scores demonstrated strong binding with FGFR1. More importantly, Ser-Ser-Gly-Lys-Phe-Leu-Arg (SSGKFLR) exhibited the most robust binding affinities, which formed interactions with FGFR1 residues via hydrogen bonds, van der Waals forces, and electrostatic interactions. The anti -sarcopenic efficacy of SSGKFLR was further validated in DEX-induced zebrafish model. Those findings indicate that WP may serve as an effective dietary intervention approach to combat sarcopenia.
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Journal of Materials Chemistry B
·
2025
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IF 5.7
Yu Li,Pei Xie,Ruixin Gong,Junlong Chen,Yaxue Liu,Zongning Yin
Rheumatoid arthritis (RA), a chronic autoimmune disorder affecting 1% globally, urgently demands advanced therapies to overcome the systemic toxicity and limited efficacy of conventional glucocorticoids like dexamethasone (Dex). In this study, we constructed LMWH-Gly-Pro-ODA/Dex (LGPO/Dex) micelles, which synergistically integrate low molecular weight heparin (LMWH)-mediated active targeting with Gly-Pro-mediated fibroblast-activated protein (FAP)-α-responsive drug release to achieve spatiotemporal precision in RA treatment. The system operates through a three-stage cascade mechanism: (1) targeting the inflamed joints, (2) inflammation-responsive drug release to modulate pathological microenvironments (e.g., normalizing M1/M2 macrophage polarization), and (3) suppression of monocyte recruitment to prevent disease progression. LGPO/Dex micelles showed excellent RA therapeutic effects in the adjuvant-induced arthritis (AIA) model. Joint swelling, serum TNF-α, and nitric oxide (NO) levels in LGPO/Dex-treated rats showed no significant difference from healthy controls (ns) while exhibiting marked improvement over Dex monotherapy (**, P < 0.01). Notably, it also significantly reduced Dex-associated adverse effects. This study confirmed the feasibility of using FAP-α as a therapeutic target for RA and provided a new idea for RA treatment, offering a blueprint for disease-microenvironment-programmed therapeutics.
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Journal of Radiation Research and Applied Sciences
·
2025
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IF 2.5
Lan Tang,Xin Zhang,Ye Huang,Depeng Kong,Yiwen Yan,Zhimin Ou,Mulan Zhu,Yi Li,Jianwei Wang
Objective This study aimed to enhance the solubility and dispersion of poorly water-soluble dexamethasone (DEX) in oral films by developing a novel pullulan-vitamin E succinate (PUL-VES) coupling compound (designated PUVS3) as the film matrix. Methods The amphiphilic coupling compound PUVS3 was synthesized, characterized and evaluated. Using PUVS3 as a solubilizing/suspension agent, and PUL as the film-forming material, a dexamethasone-fast dissolving oral film (DEX-FDOF) was prepared by solvent casting method. The film was evaluated for appearance, microstructure, mechanical properties, weight variation, content uniformity, disintegration time and in vitro dissolution. Results The DEX-FDOF formulation exhibited a smooth surface with no observable drug precipitation and demonstrated excellent transparency. Both weight variation and content uniformity complied with the pharmacopoeial standards. The film displayed rapid disintegration (<15s) and favorable mechanical properties with an elastic modulus of 35–45 MPa and elongation at break of 17%–20%. Notably, in vitro dissolution reached approximately 47 % within 10 min, representing a significant improvement over the pure drug. This enhancement was achieved through the use of a self-synthesized PUL-VES coupling compound as the film matrix. This innovative approach enabled homogeneous dispersion of the poorly water-soluble DEX within the water-soluble oral film while simultaneously improving its solubility characteristics. Conclusion The DEX-FDOF, fabricated using the self-synthesized PUL-VES coupling compound as the matrix, exhibited excellent uniformity, mechanical strength, rapid disintegration (<15 s), and notably enhanced dissolution (47 % in 10 min), demonstrating its potential as an effective delivery system for poorly soluble drugs such as DEX.
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FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8
Gongshuai Song,Tian Zhao,Yingcong Yang,Yangcheng Ge,Wei Tang,Taijiao Xiang,Danli Wang,Tinglan Yuan,Ling Li,Yong Cheng,Mengna Zhang,Jinyan Gong
The structural conversion of β-lactoglobulin (β-LG) into amyloid fibrils offers an effective strategy for developing functional biomaterials with enhanced physicochemical properties and functionalities. This study investigated the effect of cold plasma (CP) and ultrasound pretreatments on β-LG fibril (β-LGF) under acid-heat conditions (pH 2.0, 90 °C, 10 h) and explored the relationship between fibril structure and functional performance. Compared with the control, CP pretreatment significantly increased ThT fluorescence intensity by 1.9-fold, indicating enhanced fibril formation. Dynamic light scattering revealed that CP-treated fibrils (P-β-LGF) exhibited a reduced average particle size (183.6 ± 4.7 nm) and narrower distribution (PDI = 0.21) compared with ultrasound-treated (243.1 ± 6.5 nm) and control samples (278.4 ± 7.8 nm). FTIR and CD spectra confirmed the structural transition from α-helix to β-sheet, while SEM micrographs showed elongated, uniformly dispersed fibrils after CP pretreatment. Functionally, P-β-LGF exhibited the highest emulsifying activity index (51.2 m 2 /g), emulsion stability index (87.3%), and antioxidant activities, the emulsions stabilized by P-β-LGF-Dextran complex exhibited the superior thermal and ultraviolet stability of encapsulated lycopene. The highest retention rate (91.6%) was obtained in the emulsion. These findings demonstrated that CP treatment is an effective, green, and tunable strategy to regulate protein conformation and fibrillation kinetics, thereby enhancing the structural and functional properties of β-LG, providing new insights into the design of protein-based delivery systems for bioactive compounds.
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Acta Physiologica
·
2026
·Vol. 242
·期 10
·e70299
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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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ACS Applied Nano Materials
·
2025
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IF 5.5
Sifang Zhao,Fengjiao Chen,Mengxin Ban,Jian Zhou,Kerong Wu,Tengbo Yu,Bowen Chen,Lingling Zhao,Ziyu Liu
The specific targeted drug delivery is crucial for antitumor therapy. In this study, phenylboronic acid (PBA)-modified and ROS-responsive biomimetic polymeric nanoparticles have been developed for the targeted delivery of the antitumor drugs. Nanoparticles were constructed by encapsulating doxorubicin (DOX) through the self-assembly of phenylborate pinalol conjugated dextran, followed by erythrocyte camouflage and PBA modification. The particulate size of nanoparticles was 128.3 ± 11.0 nm, which increased slightly to 171.0 ± 10.4 nm after erythrocyte camouflage and PBA modification. The nanoparticles showed sustained and ROS-triggered drug release in vitro. They had excellent colloidal stability in PBS and 10% FBS due to the erythrocyte camouflage, which can help to prolong their blood circulation time. The cellular uptake of nanoparticles was remarkably enhanced due to PBA modification, and the inhibition of cell migration and cell invasion was also promoted. The nanoparticle system can effectively promote the apoptosis of B16F10 cells and show a good antitumor effect in vitro. Thus, this PBA-modified and ROS-responsive biomimetic nanoparticle system has promising application prospects as a tumor-targeted drug delivery system.
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INFLAMMATION
·
2020
·Vol. 44
·期 2
·746-757
·
IF 3.212
Gao Yang,Kang Kai,Liu Yan-song,Li Na-na,Han Qiu-yuan,Liu Hai-tao,Kong Wei-lan,Zhang Xing,Huang Rui,Yang Zhen-yu,Qi Zhi-dong,Zheng Jun-bo,Li Ming,Wang Hong-liang,Li Jia-yu,Liu Rui-jin,Wang Si-cong,Zhang Wei-hua,Zhao Ming-yan,Yu Kai-jiang
This study aimed to investigate the effect of splenectomy on dexmedetomidine-activated cholinergic anti-inflammatory pathway-mediated alleviation of LPS-induced AKI. A mouse model of septic kidney injury was established in C57BL/6 mice. A total of 30 C57BL/6 mice were randomly divided into the control group, LPS group, dexmedetomidine + LPS group, splenectomy group, splenectomy + LPS group, and splenectomy + dexmedetomidine + LPS group. The pathological effects in kidney tissues in each group were analyzed by HE staining. Apoptosis in each group was examined by the TUNEL method. Cr and Cys-C levels in each group were measured by ELISA. The expression levels of IL-6, NF-κB p65, Caspase-3, the antiapoptotic protein Bcl-2, the proapoptotic protein Bax, and α7nAChR in each group were measured by qRT-PCR and Western blotting. Dexmedetomidine alone reduced apoptosis in kidney tissue; however, apoptosis was increased after splenectomy in mice treated with dexmedetomidine. Splenectomy reduced the production of proinflammatory cytokines in circulation and had a protective effect on the kidney. Splenectomy inhibited dexmedetomidine-mediated activation of the α7nAChR pathway. Dexmedetomidine effectively alleviated LPS-induced kidney injury, and splenectomy inhibited the anti-inflammatory, antiapoptotic, and renoprotective effects of dexmedetomidine. The kidney-spleen axis is mediated by the α7nAChR-NF-κB signaling pathway and is involved in the development of AKI.
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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
·
2025
·Vol. 29
·期 6
·e70372
·
IF 4.2
Wang Huikang,Cao Shiya,Pan Di,Faisal Ayub Kiani,Li Hao,Nan Sha,Lin Xuan,Mahmoud M. Abouelfetouh,Zulfiqar Ahmed,Ding Mingxing,Ding Yi
Neuropathic pain (NP), resulting from nerve damage, is difficult to manage and often requires long-term treatment. However, prolonged use of pain medications can lead to addiction and reduced effectiveness over time. Understanding drug tolerance is essential for developing improved pain management strategies. Dexmedetomidine (DEX) is effective in targeting the α2 -adrenergic receptor, providing relief from pain, especially NP. However, its extended use leads to tolerance and hinders its clinical utility. Herein, we investigated tolerance mechanisms and potential applications of this drug in managing NP. Adult C57BL/6 mice (male) were distributed into DEX Dosage Groups ( n = 48), DEX Tolerance Model Groups ( n = 32), SGK1 Inhibitor GSK650394 Groups ( n = 48), and NF - κB Inhibitor PDTC Groups ( n = 32) to explore dexmedetomidine's effects on NP and tolerance mechanisms. NP was established via selective ligation of the sciatic nerve branch (SNI), followed by administration of DEX. The results revealed a dose-dependent analgesic effect of DEX, with significant increases in pain thresholds observed compared to the sham group ( p < 0.05). Optimal efficacy was found at a dose of 30 μg/kg, indicating its potential as an effective treatment for NP ( p < 0.05). However, continuous administration of DEX over 13 days induced analgesic tolerance, evidenced by an initial increase in pain thresholds followed by a gradual decrease ( p < 0.05). Despite an initial efficacy in elevating pain thresholds, the analgesic effect of DEX diminished over time, returning to pre-dose levels after 5 days ( p < 0.05). Transcriptome sequencing of spinal cord samples from mice receiving multiple DEX injections revealed differential gene expression patterns, notably upregulation of SGK1 , NR2A , and NR2B subunits ( p < 0.05). Inhibiting SGK1 mitigated DEX-induced tolerance, suggesting its involvement in tolerance development ( p < 0.05). Moreover, NF - κB inhibition reversed DEX-induced tolerance and implicated the SGK1 - NF - κB pathway in the mediation of analgesic tolerance. To sum up, these findings revealed the molecular mechanism underlying DEX-induced analgesic tolerance in the NP model and offer potential avenues for future therapeutic interventions.
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