International Journal of Biological Sciences
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2026
·Vol. 22
·期 12
·6790
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IF 11.7
Wentao Xie,Hongsen Liao,Yali Dai,Lin Chen,Yujie Li,Zhuo Cheng,Chunmeng Shi
Radiation-induced lung injury (RILI) is a common complication of thoracic radiotherapy and can be critically exacerbated by pre-existing pulmonary inflammation, yet the synergistic mechanisms driving this pathology remain elusive. Using a murine model of combined lung injury induced by lipopolysaccharide (LPS) and thoracic irradiation (IR), we identified macrophage extracellular traps (METs), a type of web-like chromatin structure released by macrophages, rather than neutrophil extracellular traps (NETs), as a prominent pathogenic process. Mechanistically, the combination of LPS and irradiation induced an early endothelial senescence-associated phenotype and a CXC chemokine-enriched secretory profile. These signals engaged macrophage CXCR2, leading to p38/ERK pathway activation and reactive oxygen species (ROS) production that contributed to METs formation (METosis). Functionally, METs serve as potential dual-phase mediators, contributing to epithelial barrier disruption during acute injury and promoting epithelial-mesenchymal transition (EMT)-like epithelial remodeling, thereby potentially linking early inflammatory damage to subsequent fibrotic progression. Furthermore, we demonstrate that the bioactive compound Cordycepin exerts protective effects by suppressing p38/ERK pathway activation and attenuating METosis. Collectively, these findings support a potential endothelial senescence-associated secretory signaling-METosis axis, providing a novel mechanistic framework and candidate therapeutic strategies for managing high-risk radiation-induced lung injury.
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Journal of Functional Foods
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2026
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IF 3.9
Jia-fan Liang,Dong-liang Wang,Zhi-hui Zhang,Yi-xuan Li,Man Yuan,Meng-meng Ju,Ya-nan Sun,Guo-ping Zhao
Inflammatory bowel disease (IBD) is a chronic condition associated with epithelial barrier disruption, dysregulated immunity, and gut microbiota imbalance, with substantial morbidity and mortality rates. Effective treatments without side effects are limited, highlighting the need for alternatives. Edible bird's nest (EBN), a traditional health food rich in sialic acid (SA), exhibits antioxidant, immunomodulatory, and gut barrier–enhancing activities. Its effects and mechanisms against intestinal inflammation are unknown. Here we evaluated the effects of EBN on lipopolysaccharide (LPS)-induced colitis in male C57BL/6 J mice. EBN significantly attenuated LPS-induced intestinal inflammation, reduced intestinal permeability, and alleviated colonic tissue damage in a dose-dependent manner. It also increased IL-6 level and promoted M2 macrophage polarization. Furthermore, EBN altered gut microbiota composition, notably increasing the relative abundance of Blautia. Spearman correlation analysis identified strong associations between inflammatory cytokines (IL-1β, IL-6, IL-10) and beneficial taxa such as Blautia and Roseburia. These findings indicate that EBN exerts significant protective effects against LPS-induced intestinal inflammation, with SA likely acting as a key bioactive component. This work provides evidence supporting the potential of EBN as a dietary intervention for IBD treatment.
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DIABETES OBESITY & METABOLISM
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2026
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IF 6.1
Xingyu Yang,Linglong Zhang,Xiao Li,Yue Wu,Ziwei Yu,Xinyue Jing,Tiancheng Xu,Zhi Yu,Bin Xu,Li An,Mengjiang Lu
Aim Obesity impairs the colonic mucus layer and disrupts intestinal barrier function, leading to chronic inflammation. This study explores whether electroacupuncture can restore intestinal barrier integrity and alleviate chronic intestinal inflammation by promoting goblet cell mucus secretion via the TRPV1–CGRP–RAMP1 axis. It also examines the underlying mechanisms of sensory neuron. Epithelial cell crosstalk in this process, with the goal of providing a new interventional strategy for treating obesity-related intestinal barrier damage and metabolic inflammation. Materials and Methods In a high-fat diet (HFD)-induced obesity model using C57BL/6J mice, we employed tissue-clearing techniques to examine the expression of TRPV1 and CGRP in intact colon tissue. The expression of RAMP1 in goblet cells was assessed by immunohistochemistry. Colon pathology was evaluated using immunofluorescence, haematoxylin and eosin (H&E) staining, and Alcian blue-periodic acid-Schiff (AB-PAS) staining. Furthermore, western blot analysis was performed to measure the expression levels of tight junction proteins and proinflammatory cytokines in the colon tissue. Results HFD feeding resulted in increased intestinal permeability and aggravation of intestinal inflammation. Notably, electroacupuncture intervention reversed HFD-induced intestinal pathologies. Through targeted ablation of TRPV1 and administration of the RAMP1 antagonist BIBN4096, we further established the essential roles of TRPV1 signalling and the CGRP receptor RAMP1 in maintaining mucus layer thickness and intestinal homeostasis. Under these conditions, the therapeutic efficacy of electroacupuncture was abolished. Conclusions We demonstrated that electroacupuncture may promote mucus secretion from goblet cells via the TRPV1-CGRP-RAMP1 axis, thereby suppressing intestinal inflammation. This provides a feasible interventional strategy for treating obesity-related intestinal barrier damage.
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Foods
·
2026
·Vol. 15
·期 14
·2550
·
IF 6
Yuhan Jiang,Sha Ao,Xianwen Hu,Shilin Liu
Water-in-water (W/W) Pickering emulsions based on aqueous two-phase systems (ATPS) are promising for food applications, but their stabilization is challenged by the ultra-low interfacial tension inherent to ATPSs. This study developed food-grade W/W Pickering emulsions stabilized by bacterial cellulose nanocrystals (BCNCs) and evaluated their ability to regulate starch digestibility. The effects of dextran (Dex) concentration, maltodextrin (MD) concentration, and BCNC content on the microstructure, rheological properties, and stability of the emulsions were systematically investigated. The partitioning behavior of amylopectin (AMP) between the two phases and the in vitro digestion behavior of AMP-loaded W/W Pickering emulsions in the presence of α-amylase were further examined. Fourier-transform infrared spectroscopy confirmed the successful preparation of BCNCs. The optimal formulation (24 wt% Dex, 14 wt% MD, and 0.24 wt% BCNCs) exhibited a uniform droplet distribution and enhanced storage stability. Contact angle analysis indicated preferential wettability of BCNCs toward the continuous Dex-rich phase, promoting interfacial adsorption and droplet stabilization. The emulsions remained stable at pH 3.0–7.0 but were sensitive to ionic strength above 7 mM sodium chloride. Importantly, in vitro digestion showed that BCNC-stabilized emulsions significantly inhibited α-amylase-mediated hydrolysis of AMP, with the hydrolysis extent reducing from ~54% to 14%. These results indicate that BCNCs act as effective natural stabilizers for W/W Pickering emulsions, forming a physical barrier that retards starch digestion. This work provides a sustainable strategy for designing slow-digestible, low-glycemic-index food systems with potential applications in functional foods and pharmaceuticals.
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JOURNAL OF MATERIALS SCIENCE
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2026
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IF 4.4
Wu Shuang,Li Xiaoyu,Xu Jiayi,Zeng Rong
Microneedle patch (MNP) technology offers a promising strategy for effectively transdermal delivery of macromolecular agents for treating various diseases, in particularly, dissolvable MNPs containing liposomes with tunable physicochemical properties have received widespread attention for improving macromolecular therapeutic efficacy. However, their design and optimization remain challenging. In this work, a series of liposomes with different size and modulus (100 vs. 500 nm, ~ 0.2 vs. ~ 100 kPa) were prepared and then integrated with poly( γ -glutamic acid) ( γ -PGA) to form dissolvable MNPs containing liposomes with good loading capacity, mechanical properties and biocompatibility via centrifugation-assisted micromolding for transdermal macromolecular delivery, and more uniformly dispersed liposomes appeared in the microneedle matrix for smaller liposomes (100 nm). Using FITC-dextran as the model macromolecule loaded in liposomes (100 nm) in PGA-based MNPs, in vitro and in vivo transdermal experiments revealed that MNPs containing liposomes were beneficial for improving macromolecular therapeutic efficacy, and low-modulus liposomes (~ 0.2 kPa) delivered had a more pronounced effect on the extension of the retention duration and region of macromolecular cargo in skin than high-modulus liposomes (~ 100 kPa) possibly due to their lower macrophage uptake and stronger diffusion ability. Our findings will be useful to guide the design and construction of MNP-based transdermal macromolecular composite-delivery systems. Graphical abstract
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Science China-Life Sciences
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2026
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IF 9.6
Zhuo Yingying,Yan Sen,Zhang Zhiwei,Dong Bangjian,Yin Dandan,Wen Yongping,Mao Yuejian,Zhang Zhipeng,Wang Kai,Jiang Changtao
Gut microbiota is known to interact with the host to modulate homeostasis and disease. Recent studies have shown that gut microbiota can produce enzymes, such as dipeptidyl peptidase 4 (DPP4), that perform functions similar to host enzymes, thus acting as “microbial-host-isozyme” within the host. However, the strain specificity and substrate adaptability of microbiota-derived DPP4 both remain poorly characterized, and the potential implications of microbiota-derived DPP4 on the host remain unclear. Here, we screened different microbiota-derived DPP4s for their enzymatic activities and substrate adaptability, and characterized a specific regulatory effect of Bacteroides vulgatus -derived DPP4 (BvDPP4) on GLP-2. We found that BvDPP4 could disrupt the intestinal barrier and aggravate colitis by inactivating GLP-2. Moreover, we conducted a screen of natural products and identified theaflavin as an inhibitor of BvDPP4, which also regulates levels of GLP-2. Notably, treatment with theaflavin could ameliorate BvDPP4-induced worsening of colitis in a preclinical model. Taken together, our results demonstrate that gut microbial enzymes are therapeutic targets that can be modulated by treatment with natural products, such as theaflavin, to improve gut health. Moreover, our activity-based screening strategy represents an innovative new approach for characterizing microbial enzymes in host disease.
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IMMUNOLOGY
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2026
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IF 5.4
Sisi Zhang,Zhou Jingxiang,Caixia Tan,Yuanyuan Xiao,Ju Zou,Biyue Tian,Anhua Wu,Chunhui Li
Clostridioides difficile infection (CDI) remains a major cause of antibiotic-associated colitis and is characterized by excessive intestinal inflammation, epithelial barrier disruption and impaired mucosal repair. Although sodium butyrate (NaB), a microbiota-derived short-chain fatty acid, has demonstrated anti-inflammatory and barrier-protective properties, the immunological mechanisms underlying its protective effects during CDI remain incompletely understood. In this study, we investigated the role of NaB in regulating macrophage polarization and epithelial repair using murine CDI models, primary bone marrow-derived macrophages, THP-1-derived macrophages, Caco-2 epithelial cells and macrophage–epithelial co-culture systems. NaB treatment significantly alleviated CDI-associated weight loss, colonic shortening, histopathological injury and inflammatory cytokine production while restoring epithelial barrier integrity and tight junction protein expression. Mechanistically, NaB promoted macrophage polarization towards an anti-inflammatory M2 phenotype, characterized by increased CD206 and IL-10 expression and reduced CD86 and IL-1β expression. These immunomodulatory effects were accompanied by suppression of PI3K/Akt/mTOR signalling in both colonic tissues and macrophages. Pharmacological inhibition and activation studies further supported the involvement of this pathway in NaB-mediated macrophage reprogramming. Importantly, conditioned medium from NaB-treated macrophages enhanced epithelial viability, migration and barrier-associated protein expression, whereas IL-10 neutralization partially abolished these protective effects, highlighting a critical role for macrophage–epithelial crosstalk. Collectively, our findings demonstrate that low-dose NaB protects against CDI-induced intestinal injury through coordinated regulation of macrophage polarization and epithelial barrier repair, at least in part via modulation of PI3K/Akt/mTOR signalling. These results identify NaB as a promising host-directed therapeutic strategy for CDI and provide new insights into microbiota-derived metabolite–immune interactions during intestinal inflammation.
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ACS Nano
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2026
·
IF 17.3
Jie Luo,Yu Tang,Hongzhao Yang,Shuang Zhao,Ping Huang,Zuowei Xie,Jingsen Cao,Jiaqi Liu,Jing Sheng,Ruijia Deng,Ben Niu,Meilin Gong,Dan Luo,Xiaoqi Tang,Ming Chen,Kai Chang
DNA hydrogels are promising materials for biosensing, but translating their molecular recognition capabilities into portable diagnostics is hindered by slow target diffusion, signal constraints, and bulk architecture. Here, we present a smart DNA hydrogel-responsive sensing platform termed Q-RAPID (Quick Response Analysis for Pathogen Identification Device) for portable nucleic acid detection. Q-RAPID integrates three functional modules. A paper-based module acts as a capillary-driven scaffold, miniaturizing the hydrogel matrix to accelerate target delivery and enhance molecular transport. A hydrogel sensing module spatially confines target-specific DNA hybridization, enabling programmable strand displacement that triggers a cascading colorimetric reaction for amplified visual output. A digital output module translates the colorimetric result into a smartphone-readable quick response (QR) code, allowing for automated classification and wireless reporting via integrated algorithms. In tests with a viral pseudovirus model and 100 clinical specimens, Q-RAPID identified target nucleic acids with 91% sensitivity, 97.3% precision, and 95% concordance were observed in the pseudovirus combination tests. The platform’s reconfigurable design allows detection of diverse respiratory pathogens and could broaden the reach of rapid molecular diagnostics in various healthcare settings, including resource-limited environments.
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Cell Host & Microbe
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2026
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IF 23.2
Junxia Zhang,Changyun Liu,Yupeng Wang,Yusi Chen,Haibao Shang,Wen Zheng,Li Jin,Peng Xie,Yingjia Li,Yahan Liu,Yunxiao Zhang,Yang Wang,Wei Zhao,Han Xiao,Guisong Wang,Xin Zhang,Xiaolei Yang,Erdan Dong,Yan Zhang
Ischemia/reperfusion (I/R) injury is a key driver in cardiomyocyte loss and cardiac dysfunction in ischemic heart disease. Here, we uncover a previously unrecognized gut microbiota-mediated mechanism that contributes to myocardial I/R injury. Using murine I/R models and fecal microbiota transplantation, we demonstrate that the gut microbiota mediates cardiac damage through selective enrichment of Bacteroides acidifaciens ( B. acidifaciens ) following I/R-induced intestinal hypoxia and elevated luminal lactate levels. B. acidifaciens produces dipeptidyl peptidase 4 (BaDPP4), which degrades cardioprotective peptides (e.g., glucagon-like peptide-1 [GLP-1]) in the plasma, amplifying myocardial injury. Pharmacological inhibition of BaDPP4 with daurisoline, a microbial DPP4-specific inhibitor, mitigates cardiac dysfunction. In acute myocardial infarction patients with I/R injury, B. acidifaciens abundance and BaDPP4 levels correlate with clinical markers of cardiac damage. Together, these findings reveal a gut-heart axis whereby microbial-derived DPP4 exacerbates cardiac I/R injury and highlight the hypoxia-lactate-BaDPP4 axis as a promising target for microbiota-based cardioprotection.
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PHYTOTHERAPY RESEARCH
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2026
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IF 8.1
Bingyu Chen,Ke Liu,Yaya Guo,Jingwei Zhao,Yanhua Wang
The global incidence of ulcerative colitis (UC), a chronic inflammatory bowel disease, is rising. Epi-berberine (EPI), an alkaloid from Coptidis Rhizoma , shows potential for UC treatment. This study aimed to assess EPI's effect on UC and explore the mechanism underlying its UC-alleviating effect. The therapeutic effects of EPI on UC were validated in dextran sulfate sodium (DSS)-induced colitis mice and lipopolysaccharide (LPS)-induced Caco-2 inflammatory models and further investigated the underlying mechanism. In vivo, high-dose EPI (200 mg/kg) attenuated weight loss, reduced disease activity index, increased colon length, lowered colon macroscopic/histological scores, restored intestinal mucosal barrier and inhibited colonic inflammation. EPI (25/50 μM) had similar in vitro effects. mRNA-seq identified EPI-regulated genes in UC mice, revealing six gene clusters with analogous expression patterns. The largest cluster contained genes upregulated by DSS but downregulated by EPI, potentially involved in the MAPK pathway. Key DEGs were enriched in PI3K-Akt and MAPK pathways, verified in vivo and in vitro. Literature retrieval and molecular docking predicted glutaminyl-peptide cyclotransferase (QPCT) as EPI's potential UC therapeutic target. EPI inhibited DSS/LPS-induced QPCT upregulation in vivo and in vitro; QPCT knockdown suppressed inflammation and preserved Caco-2 monolayer barrier function, while QPCT overexpression reversed EPI's therapeutic effects. QPCT mediates PI3K-Akt/MAPK activation, and its overexpression abrogated EPI's inhibitory effects. EPI alleviates murine UC by protecting the intestinal mucosal barrier and inhibiting inflammation, likely via regulating the QPCT-PI3K-Akt/MAPK pathway. It provides a preclinical basis for developing prophylactic strategies for inflammatory bowel disease.
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NEUROCHEMICAL RESEARCH
·
2026
·Vol. 51
·期 2
·103
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IF 4.5
Du Chaonan,Wu Yong,Geng Yuanming,Ali Alleyar,Li Zhenxing,Liu Zhiwei,Ma Chiyuan
Brain edema is a major contributor to secondary injury following intracerebral hemorrhage (ICH). Neurochemical disturbances, including disruption of blood-brain barrier (BBB) tight junctions and altered aquaporin-4 (AQP4) polarization, are central to post-hemorrhagic fluid imbalance. However, their association with glymphatic dysfunction and tissue-level alterations remains incompletely understood. A rat model of ICH was established and treated with glibenclamide. BBB integrity, glymphatic function, and AQP4 polarization were systematically evaluated using molecular, histological, and tracer-based approaches. Brain edema and perihematomal tissue mechanical properties were assessed. ICH was associated with marked disruption of BBB integrity, characterized by reduced tight junction protein expression and increased permeability, along with impaired AQP4 polarization and diminished glymphatic influx and clearance. These coordinated neurochemical alterations were accompanied by secondary changes in cerebrospinal fluid composition, brain water accumulation, and tissue mechanical properties. Glibenclamide treatment was associated with preservation of tight junction protein expression, restoration of AQP4 polarization, and improved glymphatic transport dynamics, accompanied by attenuation of edema formation and partial normalization of perihematomal tissue mechanics. Functional performance was correspondingly improved in treated animals. These findings indicate that experimental ICH was accompanied by coordinated changes in BBB integrity, AQP4 polarization, and fluid transport dynamics. Glibenclamide treatment was associated with parallel improvements across molecular, physiological, and functional domains. Collectively, the data highlight a coordinated pattern of neurovascular and fluid homeostasis alterations that may be involved in edema progression after hemorrhagic injury.
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2026
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IF 6.6
Weilong Cheng,Yanbo Wang,Yixuan Li,Guoping Zhao
Imidacloprid, a neonicotinoid pesticide that was reported to induce intestinal damage at low doses, necessitating effective intervention strategies. As a common component in food, glycine (GLY) has the capacity to alleviate intestinal damage. However, whether it can relieve the damage caused by imidacloprid leave to be clarified. This study investigated the protective effects of GLY (2% and 5%) against imidacloprid induced (0.06 mg/kg bw/day) intestinal injury in male Wistar rats. GLY supplementation attenuated intestinal permeability and enhanced the expression of tight junction proteins. Further, the pregnane X receptor-myosin light chain 2 signaling pathway that mediating imidacloprid-induced intestinal toxicity was also found repaired. GLY intervention increased the enzyme activities of cytochrome P450 3A4 and glutathione-S-transferase, which were responding for phase I and phase Ⅱ imidacloprid metabolism. Meanwhile, reduced levels of imidacloprid and its phase I metabolites, as well as increased phase Ⅱ detoxifying glutathione conjugates, both suggesting the protective role of GLY intervention through enhancing imidacloprid detoxification metabolism. Importantly, the amino acid signaling pathway related fecal metabolic profiles and microbiota composition in imidacloprid treated rats were also modulated and improved by GLY. Totally, our findings demonstrated the protective effect of GLY on intestinal damage caused by imidacloprid exposure, which provided ideas for preventing and controlling the toxicity of food contaminants.
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