JOURNAL OF BIOLOGICAL CHEMISTRY
·
2021
·
IF 5.157
Lei Chen,Miao Hao,Jingmin Yan,Lin Sun,Guihua Tai,Hairong Cheng,Yifa Zhou
Heat-modified citrus pectin, a water-soluble indigestible polysaccharide fiber derived from citrus fruits and modified by temperature treatment, has been reported to exhibit anticancer effects. However, the bioactive fractions and their mechanisms remain unclear. In this current study, we isolated an active compound, trans-4,5-dihydroxy-2-cyclopentene-l-one (DHCP), from heat-treated citrus pectin, and found that is induces cell death in colon cancer cells via induction of mitochondrial ROS. On the molecular level, DHCP triggers ROS production by inhibiting the activity of succinate ubiquinone reductase (SQR) in mitochondrial complex II. Furthermore, cytotoxicity, apoptotic activity, and activation of caspase cascades were determined in HCT116 and HT-29 cell-based systems, the results indicated that DHCP enhances the sensitivity of cancer cells to tumor necrosis factor–related apoptosis-inducing ligand (TRAIL), with DHCP-induced ROS accounting for the synergistic effect between DHCP and TRAIL. Furthermore, the combination of DHCP and TRAIL inhibits the growth of HCT116 and HT-29 xenografts synergistically. ROS significantly increases the expression of TRAIL death receptor 5 (DR5) via the p53 and C/EBP homologous protein pathways. Collectively, our findings indicate that DHCP has a favorable toxicity profile and is a new TRAIL sensitizer that shows promise in the development of pectin-based pharmaceuticals, nutraceuticals, and dietary agents aimed at combating human colon cancer.
研究领域:
肿瘤学
·
药理学
·
分子生物学
·
细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2026
·
IF 11
Yang Chen,Li Zhu,Wei Xu,Qi Chen,Fei Teng,Kaiwen Bao,Lu Zhang,Yuan Wang,Wei Wu,Zhiqiang Wang
Esophageal cancer (EC) remains a highly aggressive malignancy with limited therapeutic options and poor prognosis. To address the shortcomings of conventional therapies, we developed a biomimetic, reactive oxygen species (ROS)-responsive nanoprodrug for synergistic photothermal–chemotherapy of EC. Tannic acid and ellagic acid were chemically linked via boronate ester bonds to form a polyphenol-based nanoparticle (TPE). The epidermal growth factor receptor (EGFR)-targeting peptide GE11 was subsequently introduced onto red blood cell membranes (RBCM) to obtain GE11-RBCM, which was then used to cloak the TPE nanoparticles, yielding GE11-RBCM@TPE. The resulting nanoplatform exhibited excellent photothermal conversion capability under near-infrared irradiation and selectively released the therapeutic payload in response to elevated ROS levels within the tumor microenvironment. In vitro studies showed enhanced cellular uptake in EGFR-overexpressing EC cells and markedly increased cell death following combined photothermal and chemotherapeutic treatment. In vivo, GE11-RBCM@TPE significantly inhibited tumor growth with negligible systemic toxicity and prolonged blood circulation. Transcriptomic analysis further revealed up-regulation of pro-apoptotic ( PER1 , HK2 , BMF , DAPK2 ) and autophagy-related genes ( ATP6V0D2 , HDAC10 , BNIP3 , DEPP1 , ATG9B , NAT16 ), while SQSTM1 and IL6 were down-regulated, indicating simultaneous activation of apoptosis and autophagy. These findings suggest that GE11-RBCM@TPE represents a promising strategy for precise and effective treatment of esophageal cancer.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2026
·
IF 11
Xin Chen,Zhongxue Lin,Hao Lei,Yuan Qin,Feng Xu,Lei Xie,Zuolin Jin
Periodontitis, a chronic inflammatory disease driven by bacterial dysbiosis and oxidative stress, remains a major clinical challenge due to its complex pathogenesis and the lack of effective regenerative therapies. Here, we engineer an intelligent pH-responsive MXene-based nanosystem (MPDM) integrating polyethyleneimine (PEI) for pathogen-derived cfDNA capture, methyltransferase-like 3/14 (METTL3/14) for m6A-mediated osteogenic reprogramming, and 2,3-dimethylmaleic anhydride (DMMA) for dynamic charge-shielding to enhance targeting of inflammatory sites targeting. In vitro studies reveal that MPDM exhibits synergistic antibacterial activity, potent reactive oxygen species (ROS) scavenging capacity, and inflammation-triggered payload release. In a murine ligature-induced periodontitis model, micro-CT analysis revealed that MPDM reduced alveolar bone loss and increased the bone volume fraction by 32% (from 53% to 85%) compared to the diseased (Untreated) group. Transcriptomic analysis further reveals that MPDM downregulates toll-like receptor (TLR) and neutrophil extracellular trap (NET) formation signaling pathways, while suppressing osteoclast differentiation. By concurrently neutralizing pathogenic triggers and activating tissue repair, this work establishes a framework for next-generation nanotherapeutics in inflammatory bone disorders, with potential applicability to other multifactorial diseases.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2026
·
IF 9.6
Kai Feng,Jiajia An,Xinmiao Zhang,Gaoling Li,Yiling Ruan,Hongxiang Huang,Yanlei Sun,Xuan Liu,Xiaolian Sun
Myocardial infarction (MI) is a worldwide disease with high prevalence and mortality, but it still lacks efficient therapeutic strategies. Since it has been found that numerous cell types are involved in the pathological changes of MI, including fibroblasts, cardiomyocytes, immune cells, and endothelial cells, targeting a cell type seems no longer the ideal treatment. Here, we developed a ROS-responsive delivery system for microRNA-21 (miR-21) and DB1976 (a PU.1 inhibitor) to remodel the cardiac environment in a relatively comprehensive way. MiR-21 exhibited cardioprotective effects by improving angiogenesis, reducing apoptosis, and combating inflammation. However, the accompanying fibrosis impedes its therapeutic effect. DB1976, as a PU.1 inhibitor, could effectively inhibit fibrosis and alleviate the adverse effects of miR-21. In a mouse MI model, the hydrogel (termed mesoporous silica nanoparticles (MSN)/miR-21-DB hydrogel) significantly improved cardiac function through remodeling cardiomyocytes, macrophages, fibroblasts, and vascular endothelial cells. This work provides a new approach for repairing damaged cardiac tissue by simultaneously regulating multiple cell types in the cardiac microenvironment.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
·
2024
·
IF 10
Yujian Hui,Jiannan Mao,Min Rui,Yiyang Huang,Xinzhao Jiang,Yichang Xu,Wei Wang,Jie Wu,Liang Zhou,Kun Xi,Lixin Huang,Liang Chen
The healing of bone defects among diabetic patients presents a critical challenge due to the pathological microenvironment, characterized by hyperglycemia, excessive reactive oxygen species (ROS) production, and inflammation. Herein, multifunctional composite microspheres, termed GMAP are developed, using a microfluidic technique by incorporating Au@Pt nanoparticles (NPs) and GelMA hydrogel to modulate the diabetic microenvironment for promoting bone regeneration. The GMAP enables the sustained release of Au@Pt NPs, which function as bimetallic nanozymes with dual enzyme-like activities involving glucose oxidase and catalase. The synergistic effect allows for efficient glucose consumption and ROS elimination concurrently. Thus, the GMAP effectively protects the proliferation of bone marrow mesenchymal stem cells (BMSCs) under adverse high-glucose conditions. Furthermore, it also promotes the osteogenic differentiation and paracrine capabilities of BMSCs, and subsequently inhibits inflammation and enhances angiogenesis. In vivo diabetic rats bone defect model, it is demonstrated that GMAP microspheres significantly improve bone regeneration, as verified by micro-computed tomography and histological examinations. This study provides a novel strategy for bone regeneration by modulating the diabetic microenvironment, presenting a promising approach for addressing the complex challenges associated with bone healing in diabetic patients.
研究领域:
材料科学
·
生物医学工程
·
再生医学
·
纳米技术
·
糖尿病研究
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF INDUSTRIAL AND ENGINEERING CHEMISTRY
·
2026
·
IF 6
Jiamin Wang,Qifa Huang,Zihao Huang,Haoyue Hou,Jiawei Hou,Kaihui Xu,Hao Yuan,Sa Zeng,Tao Meng
Pickering emulsions hold significant promise as platforms for encapsulating bioactive compounds. However, the platform is limited due to narrow UV protection spectra and the lack of reactive oxygen species (ROS) inhibition. Herein, a Pickering emulsion system stabilized by mesoporous silica particles loaded with organic UV filters is designed to protect photosensitive actives. In this tailored protective system, firstly, mesoporous silica particles loaded with different UV filters (UF@MPS) were synthesized by sol–gel method. Subsequently, these particles underwent silicification through a secondary sol–gel process, yielding silicified particles (UF@MPS@S), which not only reduces the free radicals generated by the photodegradation of the UV filters by 89.3%, but also adjusts the particle wettability to a favorable three phase contact angle of 89.6° for emulsion formation. For UVA protection, the AB@MPS@S-stabilized Pickering emulsion possesses high UVA-blocking efficiency, leading to a retention of UVA-sensitive astaxanthin that is 94% higher than that in the free group after 10-day UV exposure. For UVB protection, the OMC@MPS@S-stabilized emulsion shows UVB-blocking capacity, resulting in 91% higher retention of UVB-sensitive vitamin E compared to the free group after 10-day UV exposure. This work establishes a versatile photoprotection platform for diverse bioactive compounds with varying UV-sensitive spectra, with potential for extension into pharmaceutical, food, and cosmetic applications.
✓ 已验证
产品关联
DOI
高影响因子
Small
·
2026
·
IF 11.8
Min Zhang,Kami Hu,Liuyuan Zhu,Rui Ding,Ying Hou,Junjie Mou,Haoming Xia,Yihe Lin,Purui Zheng,Lingnv Zhan,Haiping Fang,Hui He,Chunhua Zeng,Yingying Huang,Ruoyang Chen
Chronic bacterial infections pose a therapeutic challenge in eliminating bacteria while suppressing inflammation. Conventional antibiotics are often limited by drug resistance and poor biofilm penetration, contributing to a global health threat of antibiotic misuse. Reactive oxygen species (ROS) modulation offers a promising alternative, yet requires precise balance: insufficient ROS compromises antibacterial efficacy, but excess exacerbates inflammation. Here, we present a bidirectional ROS-regulation strategy for programmed antibacterial and anti-inflammatory therapy using Au-edged cuprous oxide (Cu 2 O) nanocubes on MXene (Au-Cu 2 O/MXene). Under near-infrared (NIR) irradiation, this nanocomposite induces moderate ROS, eliminating >99% of planktonic bacteria and >97% of mature biofilms. After cessation of NIR irradiation, the nanocomposite itself switches to scavenge the residual excessive ROS in the inflammatory microenvironment, which alleviates oxidative stress. Our skin wound infection model further demonstrates that Au-Cu 2 O/MXene markedly reduces bacterial burden, suppresses inflammatory responses, and accelerates wound closure. Theoretical computations reveal that Au-capping weakens O 2 adsorption through weak O 2p-Au 5d orbital hybridization and hinders photogenerated electron transfer with high work function, suppressing ROS overproduction; it also lowers the free energy barrier for H 2 O/O 2 desorption, promoting ROS decomposition. This work offers an effective antibiotic-free immunomodulation strategy for programmed biofilm eradication, infected wound repair, and inflammation suppression via context-dependent ROS modulation.
✓ 已验证
产品关联
DOI
高影响因子
Advanced Healthcare Materials
·
2026
·
IF 11
Zhiwen Wang,Yue Xie,Jiahui Zhang,Min Yang,Zhiyue Zou,Chun Zhang
Acute kidney injury (AKI) and chronic kidney disease (CKD), despite distinct etiologies, share a common pathological axis characterized by reactive oxygen species (ROS) burst, ferroptosis activation, and sustained inflammation. Targeting this ROS–ferroptosis–inflammation cycle represents a promising therapeutic strategy; however, current nanoplatforms are limited by insufficient responsiveness and limited capacity to regulate shared pathological mechanisms across distinct renal disease models. Here, we develop an engineered ROS-responsive nanozyme by integrating diselenide-bridged organosilica, hyaluronic acid (HA)-modified cerium oxide (CeO 2 ), and a selenium-containing diselenide framework. Under oxidative stress, MON@HA-CeO 2 undergoes ROS-triggered disassembly, coupling HA-CeO 2 -mediated ROS scavenging with selenium-related GPX4 restoration to suppress lipid peroxidation, ferroptosis, and inflammatory amplification. In both glycerol-induced AKI and unilateral ureteral obstruction (UUO)-induced renal fibrosis models, the nanozyme significantly improves renal function and attenuates tissue injury, fibrosis, and inflammation. Overall, this work demonstrates a versatile strategy for targeting a shared pathological axis and provides a promising platform for the treatment of diverse renal diseases.
✓ 已验证
DOI
高影响因子
Frontiers in Pediatrics
·
2026
·
IF 2.2
Yingying Jing,Gaofeng Xian,Gang Wu,Lingna Ye,Hanshu Wang,Xiaoni Cai
IntroductionThere is a clinical contradiction between postoperative analgesia and gastrointestinal functional recovery following intestinal ischemia-reperfusion (I/R) injury.MethodsIn this study, a reactive oxygen species (ROS)-responsive nanoplatform (LA-CLX-NP) was constructed by conjugating DSPE-PEG with α-lipoic acid (LA) followed by self-assembly and encapsulation of celecoxib.ResultsThe nanoparticles exhibited uniform size, good stability, and ROS/pH dual-responsive drug release properties. In vitro, LA-CLX-NP was efficiently internalized by macrophages and, compared with free drugs, more effectively scavenged ROS, restored redox balance, and modulated inflammatory cytokines. In a mouse model of intestinal I/R injury, LA-CLX-NP significantly reduced diarrhea incidence, increased mechanical withdrawal threshold, decreased abdominal licking and scratching behaviors, preserved ZO-1 tight junctions, suppressed COX-2 overexpression, and normalized serum cytokine profiles, with superior efficacy to single agents.DiscussionThis strategy achieves on-demand delivery of celecoxib to the inflamed intestine, exerts synergistic anti-inflammatory and antioxidant effects, and thereby reconciles effective pain relief with rapid gastrointestinal recovery, offering a new approach for postoperative management of intestinal I/R injury.
✓ 已验证
DOI
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2026
·
IF 5.9
Feng Cheng,Ye Li,Jiahui Lv,Nan Wang,Fengshu Fei,Yongqiang Yang,Jien Qin,Xiaochen Wu
A ROS-scavenging and anti-inflammatory nanoplatform (Hes-CeO₂@PVP/P188) co-loaded with hesperetin and cerium oxide was constructed for dry eye disease (DED) therapy. • The nanoparticles show uniform size (~110 nm), good water solubility, high biocompatibility and negligible hemolysis. • Hes-CeO₂@PVP/P188 exerts synergistic antioxidant effect by mimicking SOD/CAT activities to scavenge ROS and preserve mitochondrial membrane potential. • In DED mice, the nanosystem reduces corneal epithelial damage, promotes tear secretion and alleviates inflammatory infiltration. • The nanoparticles inhibit TNF-α–iNOS–MMP-9 cascade and upregulate HO-1/SOD 2 , breaking the pathological vicious circle of DED. Dry eye disease (DED) is a prevalent chronic ocular disorder characterized by tear film instability and oxidative stress. Herein, a Hes-CeO₂@PVP/P188 nanoparticle system co-loaded with the natural flavonoid hesperetin (Hes) and cerium oxide nanozyme (CeO₂) was developed to achieve synergistic antioxidant and anti-inflammatory effects, thereby effectively alleviating DED. The nanoparticles exhibited a uniform size (~110 nm), good aqueous solubility, and biocompatibility. In vitro assays demonstrated that Hes-CeO₂@PVP/P188 can effectively scavenge reactive oxygen species (ROS), protect cells from H₂O₂-induced oxidative damage, promote wound healing, and preserve mitochondrial membrane potential. In a benzalkonium chloride-induced murine model of DED, the Hes-CeO₂@PVP/P188 nanoparticles significantly reduced corneal epithelial defects, enhanced tear secretion, alleviated inflammatory infiltration, downregulated pro-inflammatory cytokines (including TNF-α, iNOS, and MMP-9), and upregulated the expression of antioxidant markers (including HO-1 and SOD 2 ). The nanoparticles suppressed the TNF-α–iNOS–MMP-9 cascade and effectively broke the pathological vicious cycle of DED. Importantly, the therapeutic efficacy was comparable or superior to that of commercial 0.05% cyclosporine A eye drops in certain indicators. The Hes-CeO₂@PVP/P188 nanoparticles represented a promising dual-functional nanotherapeutic strategy for the treatment of DED. Download: Download high-res image (194KB) Download: Download full-size image Preparation and application of Hes-CeO 2 @PVP/P188 nanoparticles for the alleviation of dry eye disease.
✓ 已验证
DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2026
·
IF 5.9
I-Chen Tsai,Luhui Cai,Cheng Tian,Zihan Ni,Wenqian Ding,Yue Li,Weichang Li,Qiong Xu
A ROS-responsive injectable hydrogel for DMI delivery is developed. • DMI suppresses inflammation and oxidative stress in DPSCs. • DMI does not directly promote odontogenesis under inflammation. • DMI restores odontogenesis via macrophage-mediated modulation. • The hydrogel enhances reparative dentin formation in vivo . Pulpitis is a common inflammatory disease of the dental pulp in which excessive inflammation and oxidative stress severely compromise the regenerative capacity of dental pulp stem cells (DPSCs), posing a major challenge for successful vital pulp therapy. Herein, we report an immunometabolic strategy that combines dimethyl itaconate (DMI) with a reactive oxygen species (ROS)-responsive injectable hydrogel to modulate the inflammatory microenvironment and promote functional pulp regeneration. We demonstrated that DMI effectively suppressed lipopolysaccharide (LPS)-induced inflammatory cytokine expression and ROS accumulation in DPSCs. Notably, DMI did not directly enhance odontogenic differentiation under inflammatory conditions; instead, it indirectly restored the odontogenic potential of DPSCs by attenuating macrophage-mediated inflammation. To enable localized and sustained delivery of DMI, a dual-crosslinked SADA/CMBA hydrogel was developed based on dynamic boronic ester bonds and ionic coordination, allowing ROS-triggered drug release while maintaining structural integrity and biocompatibility. In vitro studies confirmed the hydrogel’s favorable cytocompatibility, anti-inflammatory and antioxidant effects. Furthermore, in an LPS-induced rat pulpitis model, the DMI-loaded hydrogel significantly reduced pulpal inflammation and facilitated reparative dentin formation at the pulp exposure site. Collectively, this study introduces an immunometabolic and microenvironment-responsive therapeutic design for pulpitis treatment and highlights the potential of ROS-adaptive biomaterials to enhance the outcomes of vital pulp therapy. Download: Download high-res image (130KB) Download: Download full-size image DMI@SADA/CMBA hydrogel application for treating pulpitis
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2026
·
IF 12.4
Yanyan Wang,Kaishun Qi,Youyou Li,Ruirui Wei,Yuanda Lou,Min Liu,Shengjiang Wei,Yajie Zhao,Jianping Liu,Hongliang He,Wenli Zhang
Oxidative stress and macrophage autophagy dysfunction jointly drive plaque vulnerability and rupture, ultimately leading to acute atherothrombotic cardiovascular events. However, current monotherapies based solely on antioxidant intervention or autophagy induction remain insufficient for effective atherosclerosis management. Here, we reported the development of a cationic antioxidant dextran derivative (DKT) with intrinsic reactive oxygen species (ROS)-scavenging capacity, designed to co-deliver rapamycin-loaded reconstituted high-density lipoprotein (RC-rHDL) for synergistic atherosclerosis therapy. Through electrostatic interactions, DKT mediated the assembly of small-sized RC-rHDL into large-sized nanoassemblies (RT-rHDL), enabling efficient vascular targeting and ROS-triggered disassembly within plaques. In vitro studies demonstrated that RT-rHDL nanoassemblies effectively inhibited foam cell formation, suppressed inflammation, and reduced apoptosis by combining ROS elimination with autophagy activation. In vivo, RT-rHDL nanoassemblies accumulated at atherosclerotic lesions via endothelial binding and penetrated deeply into foam cell–rich plaques. A three-month intravenous treatment in apoE −/− mice significantly reduced plaque size, minimized necrotic core areas, resolved local inflammation, and enhanced plaque stability. Mechanistic investigations confirmed that systemic and lesional oxidative stress attenuation together with macrophage autophagy restoration underpinned these therapeutic benefits. Collectively, our findings highlight the importance of simultaneously modulating cellular functions and the plaque microenvironment, offering a novel synergistic nanotherapeutic strategy for atherosclerosis treatment.
✓ 已验证
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）