CHEMICAL ENGINEERING JOURNAL
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2026
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IF 12.5
Yuxiang Li,Sheng Dong,Ran Yu,Runjie Liu,Hengxi Xu,Hainuo Li,Wenbo Ming,Guochao Liao,Rong Zhang,Zhongqiu Liu,Wenxian Wang,Xiang Luo,Kun Liu
Chronic diabetic wound exhibits persistent hyperglycemia-associated oxidative stress and unresolved inflammation, which together impair the transition from inflammatory to regenerative phases. In this study, we propose a topology-coupled molecular integration strategy to construct microenvironment-adaptive dynamic chitosan-derived microneedles for diabetic wound repair. Methacrylated chitosan was grafted with 4-formylphenylboronic acid and subsequently integrated with Astragaloside IV (AS) through reversible boronate ester and Schiff-base interactions, enabling the therapeutic molecule to function as a structural node within the dynamic network rather than a physically encapsulated payload. The resulting dual-crosslinked network combines permanent covalent stabilization with dynamic bond exchange, enabling structural adaptability. Under hyperglycemic and oxidative conditions, these dynamic linkages undergo bond exchange and partial dissociation, leading to network relaxation and accelerated drug release. The hydrogel exhibits enhanced viscoelasticity, stress relaxation capacity, and fatigue resistance, supporting robust microneedle penetration and sustained delivery. In vitro and in vivo studies demonstrate attenuation of AGEs accumulation, suppression of TLR4/NF-κB-mediated inflammation, promotion of M2 macrophage polarization, and enhancement of collagen remodeling and angiogenesis. These findings suggest that integrating bioactive molecules into dynamic polymer networks provides an effective strategy to couple material mechanics with immune regulation in diabetic wound repair.
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JOURNAL OF NANOBIOTECHNOLOGY
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2026
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IF 15
Yunfan Li,Kaiwen Bao,Renzheng Huan,Tian Wang,Ya Wang,Shuai Wu,Xin Chen,Jiashang Huang,Li Zhu,Jianshu Li,Haifeng Yang,Wei Wu
Glioblastoma (GBM) is one of the most aggressive malignancies of the central nervous system. Gemcitabine (GEM), a pyrimidine analogue with broad-spectrum anticancer activity, can activate the cGAS-STING pathway and alleviate the immunosuppressive microenvironment of GBM. However, its clinical application is hampered by the formidable challenge of crossing the blood-brain barrier (BBB) and accumulating at the tumor lesion. Herein, a dual-responsive biomimetic nanoprodrug (RMM@GEM NPs) was exploited to enhance the efficient BBB penetration and target cargo delivery by functionalization of glioblastoma cell membranes (MM) camouflaging and further targeting peptide RAP modification. After its selective accumulation at glioma lesion, RMM@GEM NPs accelerates GEM release under the tumor pathological stimuli of reactive oxygen species (ROS) and acidic microenvironment to robustly activate the STING signaling cascades (increased p-STING, p-TBK1, p-IRF3, and p-NF-κB). Simultaneously, cyclodextrin-mediated cholesterol depletion further suppresses PD-L1 expression and alleviates T-cell exhaustion. These findings highlight RMM@GEM NPs as a promising strategy to enhance immune responses in “cold” tumor, providing a potential candidate for efficient and safe immunotherapy in GBM.
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CHEMICAL ENGINEERING JOURNAL
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2026
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IF 12.5
Yingying Pan,Jiaying Lou,Yuqi Wang,Rongfang Dai,Miwen Zou,Danni Ma,Shengzhang Chen,Jinghao Zhou,Binyan Chen,Xiaoqiong Jiang,Pan Huang,Huaqiong Li,Fuman Cai,Dejun Yang
Pressure injuries (PIs) have emerged as a significant burden on individuals and society, lacking effective treatment due to the compromised wound microenvironment resulting from ischemia-reperfusion injury. The accumulation of excessive reactive oxygen species (ROS) is the core mechanism of delayed wound healing, which triggers a cascade of harmful events, including chronic inflammation, impaired angiogenesis, and abnormal ECM degradation. Epigallocatechin gallate (EGCG) is a natural antioxidant that has been reported to promote angiogenesis and suppress inflammation, but its application is limited by low bioavailability. Herein, we employed EGCG as a crosslinker to develop a multifunctional HA-PBA/EGCG hydrogel (abbreviated as HPE) to enhance EGCG bioavailability for PIs treatment. Specifically, HPE hydrogel was prepared by the formation of the boronic ester bonds through the reaction of EGCG and phenylboronic acid-modified hyaluronic acid, and evaluated for self-healing, injectability, antioxidant activity, biocompatibility, and pH- and ROS-responsiveness. In vitro, HPE hydrogel effectively improved cell migration and protected NIH3T3 and HUVECs from TBHP-induced oxidative damage. These effects collectively improved the PI microenvironment in vivo, activated the antioxidant Nrf2/HO-1/NQO1 pathway to reduce oxidative stress damage, promoted M2 macrophage polarization, suppressed inflammation, improved neovascularization, and enhanced collagen deposition and remodeling, accelerating tissue regeneration and wound closure. In summary, these findings highlight the pronounced therapeutic potential and effectiveness of this multifunctional hydrogel in overcoming the multifaceted challenges of chronic PI wounds.
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Nature Communications
·
2026
·
IF 18.1
Mao Congyang,Jin Wanyu,Dou Limeng,Guo Tong,Huang Jin,Wang Yi,Liu Xiangmei,Wu Shuilin,Qiao Wei,Xiang Yiming,Zhu Yizhou,Wu Jun,Yeung Kelvin Wai Kwok
The pandemic-scale progression of type 2 diabetes mellitus (T2DM) necessitates innovative interventions targeting the pathogenic triad of insulin resistance, dysregulation of lipid metabolism, and gut microbiome dysbiosis. Here, we report a synthetically bioengineered probiotic consortium (REcN-F/Ca) developed through directed metabolic adaptations of Escherichia coli Nissle 1917 (EcN) under iterative hydrogen peroxide selection, subsequently functionalized with fructooligosaccharide-calcium carbonate composites. REcN-F/Ca exhibits enhanced reactive oxygen species tolerance through upregulated antioxidant enzymes and hydrogen sulfide-mediated redox balancing, alongside improved gastrointestinal survivability. In high-fat diet-induced obese male mice, REcN-F/Ca restores gut microbiota diversity, enriches butyrogenic taxa (Lachnospiraceae and Blautia ), and rescues short-chain fatty acids depletion. Transcriptomic profiling reveals PPAR signaling activation, driving lipid metabolism and suppressing adipose inflammation. These effects translate to systemic metabolic improvements with attenuated weight gain (−25.4%), restored glucose homeostasis, and reduced insulin resistance (HOMA-IR: −73.2%) in the obesity and T2DM murine model. Our findings establish REcN-F/Ca as a synthetically engineered probiotic that simultaneously corrects intestinal ecological perturbations and reverses host metabolic dysfunction, proposing a paradigm for metabolic syndrome management.
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Journal of Environmental Chemical Engineering
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2026
·Vol. 14
·期 4
·123242
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IF 7.5
Guijuan Liu,Xiaolong Zhang,Lijuan Tan,Weixing Li
The integration of photocatalytic process with peroxymonosulfate (PMS) activation constitutes a promising strategy for eliminating organic pollutants in aqueous solutions. Despite notable advances in CoFe 2 O 4 /g-C 3 N 4 composites, studies on their application in visible-light-responsive PMS-activated tetracycline (TC) degradation remain insufficient, particularly in the systematic elucidation of the quantitative order of ROS contributions and associated mechanisms. To address this knowledge gap, a recyclable CoFe 2 O 4 /g-C 3 N 4 heterojunction photocatalyst was prepared via the sol–gel method. The composites demonstrated outstanding photocatalytic performance with 97.8% TC degradation in 60 min under visible-light irradiation. The kinetic rate constant of 0.056 min −1 , which was 3.7 and 3.2 times that of pure g-C 3 N 4 (0.015 min −1 ) and CoFe 2 O 4 (0.017 min −1 ). Moreover, the developed catalyst exhibited excellent stability along with tolerance to common anions and compatibility with various organic matrices. By coupling radical quenching experiments with ESR spectroscopy, a definitive degradation contribution order for the reactive species in this system was firstly established as: 1 O 2 > SO 4 · - > O 2 · - > h + > · OH. A plausible mechanism for TC degradation was thus put forward. It provides a viable approach for developing high-performance and durable g-C 3 N 4 -derived photocatalytic system, which can be effectively utilized in environmental remediation process.
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BIORESOURCE TECHNOLOGY
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2026
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IF 8.2
Shuhan Xing,Fanghui Chen,Jiajun Lu,Xiaolin Zhang,Xiaodong Zhao,Jing He,Wei Zou,Xiaojing Li
Directed electron transfer drove deep mineralization of refractory antibiotics in groundwater. • A ROS-enzyme cascade objectively broke recalcitrant C–F and S– N bonds. • Bioenergetic costs of electron transfer induced antibiotic resistance attenuation. • Metabolic regulation shifted oxidative stress to controlled detoxification. Synchronous mitigation of recalcitrant antibiotics and antibiotic resistance genes (ARGs) in groundwater matrices remains challenging. Here, the effects of directed electron transfer (DET) on contaminant fate and metabolic regulation were investigated in a mimetic microbial electrochemical remediation system. Results demonstrated that the degradation rate of ofloxacin and sulfachloropyridazine accelerated by 1.23–1.61 times by electrogenic respiration. The DET triggered a metabolic shift from oxidative stress response to a controlled reactive oxygen species-enzyme cascade, where catalytic hydroxyl radicals and specifically upregulated hydrolases (e.g., haloacetate dehalogenase) achieved precise cleavage of recalcitrant C–F and S– N bonds. Importantly, genomic analysis provided evidence for a metabolic competition hypothesis that the high bioenergetic cost of extracellular electron transfer ecologically selected against energy-intensive resistance mechanisms, leading to resistome attenuation. This study elucidates the metabolic trade-offs involved in controlling electron flow and enzymatic detoxification, providing a strategy for the synergistic remediation of micropollutants in simulated co-metabolic groundwater. Download: Download high-res image (211KB) Download: Download full-size image
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS
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2026
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IF 5.4
Zhi Jia,Liqiang Wang,YongLan Yang,Yuezhao Zhou,Chunfeng Zhang,Yujia Liu,Jie Liu
Modulating mitochondrial dysfunction by alleviating oxidative stress has recently emerged as a promising therapeutic strategy for Alzheimer’s disease (AD), but it ignores the fact of ROS regeneration caused by dysfunctional mitochondria. Herein, we developed a mitochondria-targeted ruthenium nanozyme, Ru@CP5-TPP, to enhance mitochondrial function by simultaneously scavenging reactive oxygen species (ROS) and eliminating damaged mitochondria. Ru@CP5-TPP was fabricated by modifying ultrasmall ruthenium nanoparticles (Ru NPs) with cationic pillar[5]arene (CP5), followed by the conjugation of the mitochondria-targeting molecule triphenylphosphine (TPP) through host-guest recognition. Under NIR-I laser irradiation, Ru@CP5-TPP can bypass the blood-brain barrier (BBB), target microglial mitochondria, and scavenge existing ROS through its intrinsic CAT-like and SOD-like activities. Moreover, by mimicking NADH oxidase (NOX), Ru@CP5-TPP catalyzes the conversion of NADH into NAD + , thereby inducing mitophagy and ultimately preventing ROS regeneration. As a result, Ru@CP5-TPP effectively alleviates mitochondrial dysfunction, inhibits Aβ deposition, relieves neuroinflammation, and ameliorates memory defects in an AD mouse model. This study provides a novel approach for the multi-target treatment of AD by leveraging the multi-enzyme activity of nanozymes. Download: Download high-res image (195KB) Download: Download full-size image Ru@CP5-TPP was constructed by modifying cationic pillar[5]arene (CP5)-capped Ru nanoparticles (Ru@CP5) with the mitochondria-targeting ligand TPP. Under NIR-I light irradiation, Ru@CP5-TPP can cross the blood-brain barrier (BBB), target microglial mitochondria, scavenge ROS, and promote mitophagy, thereby preventing ROS regeneration and ultimately alleviating Alzheimer's disease.
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International Journal of Pharmaceutics-X
·
2026
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IF 7.9
Liang He,Chenke Wei,Yukai Guo,Xinting Yang,Quan Lin,Wan Wang,Chao Zheng
Postoperative recurrence remains a major challenge in prostate cancer (PCa) treatment, and insufficient drug concentration at the tumor site represents a critical barrier to effectively suppressing tumor regrowth and lymph node metastasis. To address these limitations, we developed a photo-crosslinkable oxidized konjac glucomannan/gelatin-methacrylate hydrogel (OG@Cur) for localized and sustained delivery of curcumin (Cur) during the postoperative period. This hydrogel forms a porous and adhesive network that enables prolonged curcumin release during biodegradation while simultaneously facilitating hemostasis. Cur released from the hydrogel maintained a high local concentration at the surgical site, thereby enhancing antitumor activity through the induction of intracellular reactive oxygen species accumulation. In a postoperative PCa recurrence model, this localized and sustained delivery strategy significantly suppressed tumor regrowth and reduced lymph node metastasis, while exhibiting good biocompatibility. Overall, this hydrogel system, which continuously releases curcumin, provides an effective localized therapeutic approach for preventing postoperative prostate cancer recurrence and may offer advantages over conventional systemic therapies.
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ACS Applied Materials & Interfaces
·
2025
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IF 8.2
Yan Zhou,Xie Huang,Han Liu,Zaizhi Du,Mingquan Gao,Zhengyu Zhang,Shihao Fu,Rong Li,Qiang Xiang,Shenglin Luo
Radiation-induced skin injury (RISI) is one of the most common illnesses in external beam radiotherapy. Although some commercial drugs for external use have been developed to prevent and alleviate RISI, a majority of them usually adopt a single chemical repair pathway by scavenging intracellular toxic reactive oxygen species (ROS) with limited treatment outcomes. Particularly, the therapeutic effect toward high-dosage acute radiation injury remains unsatisfactory in the clinic. Mitochondria play vital roles not only as cellular energy factories but also as the main organelles to produce intracellular ROS and maintain the balance of oxidation stress and inflammation. Thus, targeting the protection of mitochondria from radiation-induced damage may effectively improve RISI treatment. Herein, in this work, we designed and reported a series of mitochondria-targeting radioprotective hemicyanine (HCY) small molecules to treat acute RISI synergistically by antioxidation, anti-inflammation, and plasminogen inhibition for wound healing. Using ROS-cleavable enamine bonds, different mitochondria-targeting structures of HCY were chemically conjugated with tranexamic acid (TA), a plasminogen inhibitor previously reported for attenuating RISI by the regulation of mitochondrial function. Thus, the specific delivery and release of TA in mitochondria were achieved to enhance RISI treatment and minimize the side effect. Our findings in this work not only demonstrate a promising potential of HCY-TA conjugates for RISI treatment but also propose an innovative mitochondria-targeting delivery system to hopefully mitigate radiation-induced other diseases.
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CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Hongyan Lu,Ying Cheng,Xiangling Pu,Xingtao Zhao,Ruolan Li,Ruiqi Sun,Xiaoman Xie,Mingyue Wu,Shuo Zhang,Qiong Pan,Jin Chai
Simultaneously alleviating oxidative stress and remodeling inflammatory microenvironment holds great promise for treating inflammatory bowel disease (IBD). Nevertheless, the efficacy of conventional therapies remains limited by poor targeting, insufficient modulation of the inflammatory microenvironment and serious adverse effects. Here, inspired by the intrinsic biological properties of metal-curcumin (Cur) complexes, a nanozyme-mediated ion-exchange strategy was proposed to enhance the targeted therapeutic effect of Cur for IBD. Specifically, copper-doped mesoporous polydopamine nanoparticles (Cu-mPDA) with dual enzyme-like activities were served as drug carriers to encapsulate water-soluble zinc-curcumin (Zn-Cur) and further modified with hyaluronic acid (HA), yielding Zn-Cur/Cu-mPDA@HA. Encouragingly, Zn-Cur/Cu-mPDA@HA could degrade in inflammatory microenvironment, releasing Zn-Cur and Cu 2+ , which subsequently in situ generate Cu-Cur with high antioxidant activity by ion-exchange reaction. Notably, Zn-Cur/Cu-mPDA@HA not only exhibited favorable targeting specificity toward M1 macrophages in inflamed colon tissues, but also displayed enhanced abilities to scavenge ROS, inhibit pro-inflammatory factors secretion and promote macrophages repolarization from the pro-inflammatory M1 state to the anti-inflammatory M2 subtype. Mechanistically, Zn-Cur/Cu-mPDA@HA suppressed the TLR4/MyD88/NF-κB pathway, breaking the inflammation-free radical vicious cycle, thereby attenuating chronic inflammation and fostering a favorable microenvironment for intestinal barrier restoration. Such a nanozyme-mediated ion-exchange and in situ drug generation strategy offers a new insight for designing nanomedicines for the treatment of IBD and other inflammatory diseases.
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BMC Pharmacology & Toxicology
·
2025
·Vol. 26
·期 1
·1-13
·
IF 2.7
Fu Wenying,Lu Hui,Yan Ying,Shu Chongchong,Xu Chenxin,Chen Yinghua,Xia Yiqun,Chen Jundixia,Chen Yunzhi,Zou Peng,Cui Ri,Ni Daoyong
Section
Background
Lung cancer continues to rank as a leading cause of cancer-related mortality worldwide. Despite notable advances in medical research, therapeutic options for advanced-stage lung cancer remain inadequate. Heat shock protein 90 (HSP90) has been identified as a potential therapeutic target in multiple malignancies, such as lung and colon cancers, owing to its pivotal role in stabilizing numerous oncoproteins. Nonetheless, the clinical application of HSP90 inhibitors has faced challenges, including suboptimal efficacy and the development of resistance mechanisms. B-AP15 is a promising small molecule in cancer therapy that functions by inhibiting deubiquitinating enzymes, which regulate protein degradation through the proteasome pathway. In this study, we aim to investigate its combinatorial activity with the HSP90 inhibitor tanespimycin (TAU) in lung cancer cells.
Section
Methods
The levels of the specified molecules were measured by Western blot analysis. Reactive oxygen species (ROS) levels were determined using the 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) probe. 53BP1 foci formation and C/EBP homologous protein (CHOP) expression were assessed by immunofluorescence. Autophagic flux was monitored using mRFP-GFP-tagged microtubule-associated protein 1 light chain 3 (LC3) lentivirus.
Section
Results
Our findings reveal that the combination of TAU and B-AP15 induces significant synergistic antitumor effects, characterized by substantial accumulation of ROS. This ROS accumulation serves as a crucial mediator of the enhanced therapeutic response elicited by the combination treatment. Mechanistic analyses further demonstrated that the combined treatment induces cell death via activation of endoplasmic reticulum (ER) stress and the c-Jun N-terminal kinase (JNK) pathway.
Section
Conclusion
In summary, our study provides robust evidence supporting the potential of combining TAU with B-AP15 as a viable therapeutic option for lung cancer treatment.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
·
IF 4.7
Yandi Pan,Hongdou Liu,Yuqian Liu,Tingting Zhang,Shichao Xu,Yilin Lu,Yi Lu,Liuyi Xu,Xiaoxiang Hu,Xuefeng Cao,Rendong Fang,Lianci Peng
With the increasing emergence of antimicrobial resistance, the rise of multidrug-resistant Streptococcus suis ( S. suis ) has caused a great threat on global public health. The combination of antimicrobial peptide (AMP) and antibiotics is an efficient strategy to enhance antibacterial efficacy and combat bacterial antibiotic resistance. In this study, the antibacterial efficacy of chicken-derived AMP CATH-1 combined with tetracycline against S. suis infection was investigated in vitro and in vivo . The results showed that combination of CATH-1 and tetracycline exerted effectively anti- S. suis activity, which rapidly killed all tested bacteria in 60 min. In the mice infection model, CATH-1 combined with tetracycline improved survival rate of SC19-infected mice, reduced bacterial load in different tissues and alleviated the inflammatory response as well as inflammatory damage. Furthermore, CATH-1 reduced the emergence of bacterial resistance to tetracycline. Mechanically, CATH-1 disrupted cell membrane via SEM observation and SYTO9/PI staining. CATH-1 in combination with tetracycline aggravated reactive oxygen species (ROS) accumulation and proton motive force (PMF) disruption compared to CATH-1 or tetracycline alone. In addition, CATH-1 inhibited efflux pump function. Importantly, we identified a critical gene steAB associated with biofilm formation and CATH-1 alone or in combination with tetracycline inhibited biofilm formation. Our study shows effective anti- S. suis infection of CATH-1-tetracycline synergy, which provides the basis on the development of AMP as additives to antibiotics.
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