International Journal of Nanomedicine
·
2026
·
IF 8.7
Zhiyuan Luo,Luyu Jia,Yu Tang,Yifan Huang,Zhanni Ma,Youpeng Li,Xiaojing Zhang,Pengfei Zhang,Tian Xie
Purpose Inflammatory bowel disease (IBD) is a chronic condition driven by pro-inflammatory macrophages. Although natural compounds with carbon–carbon double bonds (C=C bonds), such as β‑elemene, exhibit anti-inflammatory properties, their precise subcellular targets and mechanisms remain elusive. This study aimed to develop a targeted nanomedicine to elucidate the anti-inflammatory mechanism of β‑elemene and establish a novel therapeutic strategy for colitis.Patients and Methods We engineered a reactive oxygen species (ROS)-responsive β‑elemene nanoemulsion (ELE-NE) for targeted drug delivery. Its therapeutic efficacy and mechanism were evaluated in a murine model of dextran sulfate sodium (DSS)-induced colitis. A mitochondria-targeted, ROS-activatable near-infrared probe was also developed for in vivo imaging tracking of inflammatory foci and assessment of therapeutic efficacy.Results In DSS-induced colitis mice, ELE-NE preferentially accumulated in inflamed colon tissue and effectively alleviated disease pathology. Mechanistically, upon reaching inflammatory macrophages, ELE-NE utilized the pathological ROS surge to undergo spatially confined aggregation at mitochondrial sites. This nano-aggregation directly disrupted the electron transport chain (ETC), potently suppressing oxidative phosphorylation and reprogramming cellular energy metabolism. Consequently, this mitochondria-focused metabolic intervention attenuated M1 macrophage polarization, reduced pro-inflammatory cytokine secretion.Conclusion This is the first report demonstrating that β‑elemene acts via ROS‑triggered mitochondrial aggregation and metabolic reprogramming. We deciphered the mechanism of β-elemene, revealing that its olefinic (C=C) functional group enables bioresponsive mitochondrial aggregation and metabolic reprogramming, thereby proposing the concept of “olefinic drugs” as a distinct therapeutic class. Furthermore, we established a novel theranostic paradigm for treating inflammatory diseases using olefinic nanomedicines, enabled by a companion imaging tool for non‑invasive detection of inflammatory foci and dynamic monitoring of the treatment process.
✓ 已验证
DOI
PubMed
高影响因子
Materials Today Bio
·
2026
·
IF 11
Yinxi Li,Qinxuan Zhou,Yuxuan She,Bin Lu,Mengting Wu,Tianhao Chen,Pengcheng Ye,Li Yu,Wenzhao Liu,Hui Deng,Xiaowen Hu
Inflammatory bowel disease (IBD) is a chronic gastrointestinal disorder characterized by a self-perpetuating pathological loop, where excessive reactive oxygen species (ROS) induce mucosal inflammation, which in turn drives further ROS production. This oxidative-inflammatory cycle leads to intestinal epithelial barrier disruption and gut microbiota dysbiosis. Current immunosuppressive therapies primarily target downstream inflammation, while fail to address the foundational oxidative stress and achieve complete mucosal healing. To bridge this gap, we developed an orally deliverable nanozyme platform by anchoring cobalt oxide (Co 3 O 4 ) nanoparticles onto montmorillonite nanosheets (Co 3 O 4 @MMT). This design leverages the Co 2+ /Co 3+ redox cycling within Co 3 O 4 for efficient multi-enzymatic ROS scavenging. Furthermore, transcriptomic analysis and literature evidence suggest that the released Co 2+ ions can activate the HIF-1α pathway—a key regulator of epithelial repair. The MMT component protects the nanozyme from gastrointestinal degradation and facilitates its electrostatic accumulation at inflamed colonic sites. In murine colitis models, oral Co 3 O 4 @MMT treatment effectively alleviated disease severity, suppressed inflammation, restored barrier integrity, and rebalanced gut microbiota. This work presents an integrated oral strategy that concurrently targets oxidative stress, inflammation, and barrier restoration, offering a comprehensive therapeutic approach for IBD.
✓ 已验证
DOI
PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8.8
Xinmin Liang,Jing Han,Tianhai Liu,Yang Yu,Di Wang,Bo Wang,Dinghong Jia,Weihong Peng,Xiaolan He,Xun Liu
ROS scavenger DMTU triggered cap color fading from dark-brown to yellow in Flammulina filiformis . • Glutathione metabolism was identified as a key pathway underlying DMTU-induced color change. • DMTU upregulated glutathione synthesis and regeneration genes while downregulating melanin biosynthesis genes. The cap color of Flammulina filiformis represents a significant commercial trait, directly affecting consumer purchasing preferences and market value, making it a primary target for genetic improvement. However, the biochemical mechanisms underlying pigmentation, particularly in newly developed dark-brown strains, remain insufficiently understood. In this study, dark-brown F. filiformis was used to investigate the role of reactive oxygen species (ROS) in cap color. Exogenous application of the ROS scavenger N , N ′-Dimethylthiourea (DMTU) significantly induced the fading of dark-brown phenotype to yellow, concomitant with reduced activity of key enzymes involved in melanin biosynthesis and an increased pheomelanin/eumelanin ratio. Metabolomic analysis revealed that DMTU treatment significantly activated the glutathione metabolism pathway, with marked accumulation of pathway-associated metabolites. Further validation demonstrated that both oxidized glutathione (GSSG) and its reduced form (GSH) induced a cap fading phenotype similar to that induced by DMTU. Furthermore, quantitative real-time PCR (qRT-PCR) analysis revealed that DMTU treatment significantly upregulated the expression of genes associated with glutathione synthesis and regeneration, while downregulating the transcription levels of key genes involved in melanin synthesis. In conclusion, this study illustrates that alterations in ROS levels can profoundly affect the cap pigmentation process in dark-brown F. filiformis by modulating the glutathione-mediated redox balance. These findings elucidate the critical regulatory role of ROS-glutathione metabolism in the color formation of F. filiformis , offering a novel theoretical framework for the quality control and future breeding aimed at developing cultivars with optimized color traits and enhanced market appeal. Download: Download high-res image (198KB) Download: Download full-size image
✓ 已验证
DOI
PubMed
高影响因子
Journal of Materials Chemistry B
·
2026
·
IF 6.2
Jiahao Du,Yunyun Sun,Dong Yu,Shengwei Lu,Simin Yu,Mei Wang,Guoqing Zhou,Songxin Xu,Lei Zhang,Yefei Zhu,Longxiang Zhou
Inflammatory bowel disease (IBD) is a refractory gastrointestinal disorder characterized by sustained intestinal inflammation, mucosal barrier dysfunction, and gut dysbiosis. Excess reactive oxygen species (ROS) is a key driver of these pathological processes. Although CeO₂-based nanozymes can scavenge ROS, its clinical application is limited by poor aqueous stability. Here, we developed an oral nanozyme by co-encapsulating ultrasmall CeO₂ nanoparticles and the clinical drug 5-aminosalicylic acid (5-ASA) within liposomes. The resulting formulation (CeLA) exhibited excellent colloidal stability and robust ROS-scavenging activity, and provided marked cytoprotection against oxidative stress in vitro. In a dextran sulfate sodium (DSS)-induced colitis model, CeLA alleviated clinical symptoms, restored intestinal barrier integrity, and suppressed pro-inflammatory cytokine expression. Notably, CeLA also reshaped the dysbiotic gut microbiome by reducing pro-inflammatory bacterial taxa. This multifunctional nanozyme integrates antioxidant, anti-inflammatory, and microbiome-modulating effects, offering a promising therapeutic strategy for IBD.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL RESEARCH IN CHINESE UNIVERSITIES
·
2026
·
IF 4.7
Gao Yuxuan,Kong Qiyu,Wang Jun,Sun Fengwei,Liu Xinyu,Wang Deliang,Li Jiangao,Yang Zhen
Developing organic type I photosensitizers (PSs) that generate less oxygen-dependent reactive oxygen species (ROS) has long been recognized to be an appealing yet significantly challenging task in the field of photodynamic therapy (PDT), owing to the high oxygen dependency of conventional PDT, which impairs its overall therapeutic efficacy, particularly in hypoxic solid tumors. Herein, a molecular fluorination strategy to finely regulate PSs with bright near-infrared (NIR) fluorescence and superior type I ROS generation ability was exploited. Benefited from the improved donor-acceptor interaction, promoted intersystem crossing process, and increased spin-orbit coupling (SOC) constant, the optimal TIBT-5F simultaneously exhibits broad absorption with a larger molar extinction coefficient in the visible-light region, bright NIR fluorescence emission and stronger type I ROS generation efficiency, making TIBT-5F a promising candidate for precise NIR fluorescence-guided PDT. The as-prepared TIBT-5F nanoparticles (NPs) can quickly accumulate in the tumor site, effectively produce both type II and type I ROS and prominently suppress the tumor growth under a safe white light irradiation (40 mW/cm 2 ) with minimized systemic toxicity. This study thus offers a new insight into constructing advanced type I PSs for precise fluorescence imaging-guided tumor theranostics.
✓ 已验证
产品关联
DOI
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.7
Jiaqi Chen,Jiayue Zhao,Yibin Xu,Xianglin Fei,Shujie Xu,Binke Chen,Wenzi Wu,Jiachen Zhuang,Xiuan Zhan,Aikun Fu
Enteric Lactobacillus plays a crucial role in maintaining the intestinal barrier integrity. Lactobacillus reuteri , one of the most described probiotic species of Lactobacillus , has been shown to alleviate enteritis-associated intestinal mucosal damage by stimulating the expansion of intestinal stem cells (ISCs). However, the underlying ligand-protein interactions remain unexplored. Therefore, this study aimed to elucidate the specific molecular mechanisms by which L. reuteri and its metabolites govern ISC stemness. We employed broiler enteritis model and organoid culture to compare the probiotic effect of a wild-type (WT) L. reuteri strain and a reuterin-deficient isogenic mutant. Compared to the WT strain, the deficient strain exhibited an impaired ability to alleviate inflammation, restore the intestinal barrier, and stimulate ISC proliferation both in vivo and ex vivo, indicating that reuterin is the essential effector. Furthermore, bioorthogonal click chemistry combined with in silico molecular docking were utilized to map the direct host protein targets. We identified protein disulfide-isomerase 1 (PDIA1), an endoplasmic reticulum (ER)-resident redox-active protein, as the direct binding partner of reuterin, characterized by a strong binding affinity. The inactivation of PDIA1 by reuterin binding increased ER-derived reactive oxygen species (ROS) level, leading to the upregulation of Wnt/β-catenin pathway and the maintenance of ISCs. In conclusion, by inactivating the ER-resident PDIA1, L. reuteri -derived reuterin promoted ISC proliferation and ameliorated intestinal mucosal damage.
✓ 已验证
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.7
Zihao Huang,Jiamin Wang,Jiawei Hou,Haoyue Hou,Kaihui Xu,Hao Yuan,Sa Zeng,Tao Meng
Inorganic nanoparticles with excellent anti-ultraviolet ability such as titanium dioxide (TiO 2 ) are extensively utilized in sunscreens to protect against UV-induced skin photodamage and carcinogenesis. However, conventional TiO 2 nanoparticles exhibit inherent photocatalytic activity that generates harmful reactive oxygen species (ROS), which limits their applications as sunscreen. In this work, we firstly apply polysaccharide-polyphenol interaction to the sunscreen application of inorganic UV filters (named TiO 2 -TA-CS). Because of the synergistic effect of corn starch (CS) in enhancing TiO 2 nanoparticles dispersion and blocking ROS, TiO 2 -TA-CS exhibit the enhanced UV absorption and leverages tannic acid (TA) to achieve complete eradication of hydroxyl radicals and superoxide radicals generated by TiO 2 nanoparticles, which superiors to the previous reports of bio-safe sunscreen. Furthermore, the UV absorption capacity of TiO 2 -TA-CS Pickering emulsions is increased by a factor of 2.5 and there is no obvious cytotoxicity in the UV evaluation. Compared with commercial sunscreens, it has lower UV penetration rate and higher SPF value. In vitro studies and cell viability assays collectively confirm the excellent efficacy of the formulated sunscreen in mitigating photoaging and protecting skin cells against UV-induced damage. Therefore, the TiO 2 -TA-CS Pickering emulsions exhibit favorable biocompatibility, high UV protection, and human skin safety, providing a new strategy for sun protection and other medical applications.
✓ 已验证
DOI
PubMed
高影响因子
Biomaterials Research
·
2026
·
IF 9.8
Kai Dong,Zelin Guan,Danyang Wang,Jinyao Sun,Ying Zhang,Cuiyu You,Yuanming Xing
In the pathogenesis of ulcerative colitis (UC), inflammatory responses, mucosal injury, and gutdysbiosis form a mutually reinforcing network that perpetuates disease progression. Current clinicalinterventions can rarely modulate these pathological modules simultaneously, underscoring theurgent need for more effective therapeutic strategies. Here, we report a dual-functional nano-therapythat couples aryl-hydrocarbon-receptor (AhR) activation with on-site reactive oxygen species (ROS)scavenging. An amphiphilic copolymer, HA-TK-LA (HTL), was synthesized by grafting lipoic acid(LA) to hyaluronic acid (HA) via a ROS-cleavable thioketal (TK) linker. The copolymer self-assembles into ~130 nm nanoparticles that encapsulate the natural AhR ligand indole-3-acetic acid(IAA) with a high loading efficiency of 73%. The resulting IAA@HTL nanoparticles exhibitROS/glutathione (GSH)-triggered drug release, and are actively taken up by inflamed intestinalepithelial cells and M1 macrophages through CD44-mediated endocytosis, leading to suppressedepithelial apoptosis and macrophage repolarization toward an anti-inflammatory phenotype. Indextran sulfate sodium (DSS)-induced murine colitis, IAA@HTL specifically accumulates in theinflamed colon and markedly alleviates disease activity. Mechanistically, IAA and LA releasedfrom the nanoparticles synergistically activate AhR/CYP1A1 and Nrf2/HO-1 signaling, skewmacrophages toward an anti-inflammatory state, dampen pro-inflammatory cytokine release, andreinforce the mucosal barrier by up-regulating tight-junction proteins and IL-22 secretion. Asinflammation subsides and mucosal integrity is restored, the gut microbiota gradually returns tohomeostasis. Collectively, this study establishes a ROS-scavenging and AhR-activating nano-delivery system that achieves a “one-stone-three-birds” outcome—attenuating inflammation,repairing mucosa, and rebalancing microbiota—providing new experimental evidence andtheoretical support for UC therapy.Keywords: ulcerative colitis, AhR receptor, reactive oxygen species, active targeting, macrophages
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ANALYTICA CHIMICA ACTA
·
2026
·
IF 6.1
Xiaoyan Su,Ruifeng Zeng,Hongyu Li,Caimi Lan,Neng Jiang,Yue Ding,Jinshuai Lan,Tong Zhang,Tingzhuang Yi
Diagnostic integration technology represents a significant advancement in cancer diagnosis and treatment. The combination of fluorescence probe-based imaging methods with photodynamic therapy (PDT) offers distinct advantages due to its high sensitivity and minimally invasive nature. However, the effective detection depth and spatial resolution of fluorescence imaging are limited by light scattering effects in biological tissues. Additionally, high concentrations of GSH in the tumor microenvironment (TME) neutralize reactive oxygen species (ROS) generated by PDT, directly inhibiting therapeutic efficacy. Therefore, developing a highly sensitive, high-resolution fluorescent probe to achieve integrated tumor diagnosis and treatment is of great significance. This study developed an activatable diagnostic-therapeutic probe, MB-2O-MB. In MB-2O-MB, methylene blue (MB) served as both the photosensitizer and signal reporting moiety, while a thiols-sensitive disulfide bond was introduced as the linker and response unit. When the probe reacted with GSH in tumor regions, the disulfide bond broke, causing structural dissociation and releasing free MB molecules. Experiments demonstrated that the probe exhibited strong interference resistance, and high sensitivity (LOD = 57.99 nM) for this reaction. Furthermore, the photoacoustic (PA) signal generated upon probe activation compensated for the limited tissue penetration depth of fluorescence imaging, enabling more precise spatial localization of tumor regions. Therapeutically, upon irradiation with 660 nm near-infrared (NIR) laser light, the released MB efficiently generated singlet oxygen, effectively inducing 4T1 tumor cell death. In vivo data further validated the significant tumor suppression effect of MB-2O-MB via PDT. In summary, MB-2O-MB achieves precise tumor localization and complete eradication through the synergistic combination of NIR fluorescence/PA dual-modality imaging and PDT. This strategy simultaneously overcomes the drug resistance bottleneck and imaging limitations of conventional photodynamic therapy, paving a new pathway for constructing highly selective and potent smart diagnostic and therapeutic systems, and significantly advancing precision medicine.
✓ 已验证
DOI
PubMed
高影响因子
Journal of Materials Chemistry B
·
2026
·
IF 6.2
Ruoning Qian,Junqing Hou,Hongjun Guo,Qiang Zhang,Jiamin Lin,Yitian Zhou,Zhiqiang Bi,Jiajia Shen,Xi Yang,Shanshan Wang,Zhengguang Zhang,Ruogu Qi
Mitochondrial dysfunction plays a critical role in hepatocellular carcinoma (HCC) progression. This study develops a glutathione-responsive Pt(IV)–artesunate (ART) prodrug (Pt–ART) that co-releases cisplatin and ART in the tumor microenvironment, synergizing DNA damage and iron-dependent ROS generation for combined chemotherapy and chemodynamic therapy. The prodrug is encapsulated into a ROS-responsive, fluorinated polyethyleneimine-chlorin e6-based polycationic nanoparticle, coated with polyethylene glycol-chondroitin sulfate for enhanced tumor targeting via the EPR effect, CD44 receptor-mediated uptake, and mitochondrial accumulation. This nanoplatform effectively inhibits Drp1 expression, induces mitochondrial membrane depolarization, and demonstrates potent triple-modality therapy combining chemotherapy, chemodynamic therapy, and photodynamic therapy. Our work provides an innovative strategy integrating herbal medicine with nanotechnology to overcome limitations of conventional Pt-based therapies.
✓ 已验证
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2026
·
IF 2.5
Chunhui Shan,Qi Bing,Gang Qiu,Hui Zhang,Yingmin Chen
Galectin-3 disrupts microglial P2X7R/MerTK balance after stroke • ERK/ROS/BRD4 axis mediates Gal-3-induced P2X7R upregulation • Gal-3 promotes cGAS-STING inflammation and apoptosis via HIF1α/P2X7R • TD-139 restores P2X7R/MerTK balance and reduces cerebral infarction • Targeting Gal-3 improves motor, cognitive, and grip strength in MCAO rats This study demonstrates that Galectin-3 (Gal3) exacerbates cerebral infarction progression by modulating the P2X7R/MerTK equilibrium in microglia via the ERK/BRD4/HIF1α signaling axis, with reactive oxygen species (ROS) serving as a potential intermediate mediator linking ERK activation to BRD4 upregulation based on prior literature evidence. Single-cell transcriptomic analysis revealed that ischemia drives microglia from a homeostatic state to an activated disease phenotype, and virtual Gal3 knockout predicted corresponding downregulation of BRD4. Using a rat model of cerebral infarction, we found that the Gal3 inhibitor TD-139 significantly reduced infarct volume, promoted M2 polarization of microglia, and improved neurological function in behavioral assays. Mechanistic investigations in BV2 microglia revealed that Gal3 activates ERK1/2, leading to ROS accumulation, BRD4 upregulation, and subsequent HIF1α-mediated P2X7R transcription, while suppressing KLF4 and MerTK. This cascade increased P2X7R expression and suppressed MerTK/KLF4 expression, generating a pro-inflammatory and pro-apoptotic microenvironment. Notably, pharmacological inhibition of Gal3 enhanced efferocytosis and reduced apoptosis, whereas P2X7R blockade exerted similar neuroprotective effects. These findings identify Gal3 as a key regulator of microglial polarization via the experimentally validated ERK/BRD4/HIF1α-P2X7R signaling cascade, where P2X7R activation concurrently triggers cGAS-STING-mediated pro-inflammatory/pyroptotic responses and suppresses the KLF4/MerTK efferocytosis axis. Targeting this regulatory network could provide therapeutic benefits in cerebral infarction by shifting microglia toward the neuroprotective M2 phenotype and facilitating inflammation resolution. Targeting this pathway could provide therapeutic benefits in cerebral infarction by shifting microglia toward the neuroprotective M2 phenotype and facilitating inflammation resolution. Data were analysed using one-way ANOVA followed by Tukey's post-hoc test for multiple comparisons; P < 0.05 was considered statistically significant.
✓ 已验证
DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Ning Jiang,Fengying Yin,Qianqian Dang,Guoliang Chen,Xiaoxia Wu,Saining Wang,Xuelin Wang,Lin Sun
MOF-ABZ significantly improved apparent aqueous dispersibility of ABZ. • MOF-ABZ induced ROS-associated ICD signaling in HCC cells. • MOF-ABZ potentiated the antitumor efficacy of low-dose DOX while reducing systemic toxicity in vivo . Doxorubicin (DOX) is widely used to treat hepatocellular carcinoma, but its dose-dependent cardiotoxicity limits its clinical application. Although dose reduction can mitigate cardiac injury, it often weakens antitumor efficacy, underscoring the need for effective sensitization strategies. Albendazole (ABZ) can induce reactive oxygen species (ROS) production, which may promote immunogenic cell death (ICD); however, its poor aqueous solubility restricts therapeutic application. To overcome this limitation, γ-cyclodextrin-based metal-organic frameworks were used to encapsulate ABZ, generating MOF-ABZ for low-dose DOX sensitization. MOF-ABZ improved ABZ dispersion and induced ROS-associated immunogenic responses in HepG2 cells, as indicated by the release of damage-associated molecular patterns (DAMPs), dendritic cell maturation, and early CD8 + T-cell activation; these effects were attenuated by N -acetylcysteine. MOF-ABZ further sensitized HepG2 cells to DOX, reducing the DOX IC₅₀ from 119.5 to 91.3 ng/mL. In H22 tumor-bearing mice, the combination of low-dose DOX and MOF-ABZ achieved tumor inhibition comparable to that of high-dose DOX alone and superior to that of low-dose DOX monotherapy, with less body-weight loss, milder histological myocardial damage, and cytokine changes consistent with immunomodulatory activity. In conclusion, through efficient ABZ delivery, MOF-ABZ enhances the antitumor efficacy of low-dose DOX, and these ROS-associated immunogenic responses potentially contribute to this sensitization effect, providing a promising strategy to improve the therapeutic index of DOX in HCC models. Download: Download high-res image (174KB) Download: Download full-size image
✓ 已验证
DOI
高影响因子
危险品化学品经营许可证（带存储）