Journal of Nanobiotechnology最新文献

{"title":"Stem cells derived exosome laden oxygen generating hydrogel composites with good electrical conductivity for the tissue-repairing process of post-myocardial infarction.","authors":"Zhaoyan Xu, Wanzi Hong, Yuanxi Mo, Fen Shu, Yaoxin Liu, Yuqi Cheng, Ning Tan, Lei Jiang","doi":"10.1186/s12951-025-03289-y","DOIUrl":"10.1186/s12951-025-03289-y","url":null,"abstract":"<p><p>Acute myocardial infarction (AMI) destroys heart cells by disrupting the oxygen supply. Improving oxygen delivery to the injured area may avoid cell death and regenerate the heart. We present the creation of oxygen-producing injectable bio-macromolecular hydrogels using catalase (CAT) loaded alginate (Alg) and fibrin (Fib) incorporated with the Mesenchymal stem cells (MSCs) derived exosomes (Exo). The composite hydrogel additionally incorporates electrical stimulating qualities from gold nanoparticles (AuNPs). In vitro experiments showed that this composite hydrogel (Exo/Hydro/AuNPs/CAT) exhibits electrical conductivity similar to an actual heart and effectively releases CAT. The O_2-generating hydrogel released oxygen for almost 5 days under hypoxia conditions. We showed that after 7 days of in vitro cell culture, produces the same paracrine factors as rat neonatal cardiomyocytes (RNCs), rat cardiac fibroblasts (RCFs), and Human Umbilical Vein Endothelial Cells (HUVECs), imitating capillary architecture and function. Our work demonstrated that the injectable conductive hydrogel loaded with CAT and AuNPs reduced left ventricular remodeling and myocardial dysfunction in rats after MI. Exo/Hydro/AuNPs/CAT boosted infarct margin angiogenesis, decreased cell apoptosis, and necrosis, and elevated Connexm43 (Cx43) expression. The therapeutic benefits and the ease of production of oxygen make this bioactive injectable conductive hydrogel an effective therapeutic agent for MI.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"213"},"PeriodicalIF":10.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional nanozyme system for synergistic tumor immunotherapy via cuproptosis and ferroptosis activation.","authors":"Lina Gu, Ying Sun, Tingjie Bai, Sijie Shao, Shumin Tang, Panpan Xue, Wanlin Cai, Xian Qin, Xuemei Zeng, Shuangqian Yan","doi":"10.1186/s12951-025-03284-3","DOIUrl":"10.1186/s12951-025-03284-3","url":null,"abstract":"<p><p>Elevated copper levels induce tumor cuproptosis and ferroptosis, leading to immunogenic cell death and subsequent antitumor immune responses. However, dysregulated copper metabolism in tumor cells maintains homeostatic copper balance, while hypoxic microenvironments hinder therapeutic efficacy. In this study, we present a nanozyme system, termed CussOMEp, comprising a copper-based nanovector (CussNV) that is PEGylated and loaded with omeprazole, a copper transporter inhibitor, to enhance tumor synergistic immunotherapy by promoting cuproptosis and ferroptosis. CussNV is assembled from dithiodiglycolic acid and copper ions, exhibiting peroxidase, glutathione oxidase, and catalase-like activities, along with responsive degradability. This nanozyme alleviates tumor hypoxia by producing oxygen, induces ferroptosis through the generation of lethal hydroxyl radicals, and depletes glutathione. Additionally, omeprazole increases cellular copper concentration and oxidative stress by inhibiting the intracellular copper-transporting ATPase 1 (ATP7A), enhancing lipoylated protein oligomerization and cuproptosis. In a breast tumor mouse model, CussOMEp elicits robust antitumor immune responses, including dendritic cell maturation and T cell proliferation. When combined with PD-1 antibodies (αPD-1), CussOMEp significantly inhibits tumor metastasis in bilateral and lung metastatic models. This work presents a functional nanozyme system as a promising strategy for synergistic tumor immunotherapy leveraging ferroptosis and cuproptosis.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"212"},"PeriodicalIF":10.6,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Eobania vermiculata whole-body muscle extract-loaded chitosan nanoparticles enhanced skin regeneration and decreased pro-inflammatory cytokines in vivo.","authors":"Alyaa Farid, Adham Ooda, Ahmed Nabil, Areej Nasser, Esraa Ahmed, Fatma Ali, Fatma Mohamed, Habiba Farid, Mai Badran, Mariam Ahmed, Mariam Ibrahim, Mariam Rasmy, Martina Saleeb, Vereena Riad, Yousr Ibrahim, Neveen Madbouly","doi":"10.1186/s12951-025-03296-z","DOIUrl":"10.1186/s12951-025-03296-z","url":null,"abstract":"","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"210"},"PeriodicalIF":10.6,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11908061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nickel-based nanomaterials: a comprehensive analysis of risk assessment, toxicity mechanisms, and future strategies for health risk prevention.","authors":"Xiaoting Zhou, Jiaqi Liao, Zipeng Lei, Huiqin Yao, Le Zhao, Chun Yang, Yan Zu, Yuliang Zhao","doi":"10.1186/s12951-025-03248-7","DOIUrl":"10.1186/s12951-025-03248-7","url":null,"abstract":"<p><p>Nickel-based nanomaterials (NBNs) have seen a surge in usage across a variety of applications. However, the widespread use of NBNs has led to increased human exposure, raising questions about their associated health risks, both in the short and long term. Additionally, the spread of NBNs in the environment has attracted considerable attention, emerging as a vital focus for research and development. This review aims to provide an in-depth assessment of the current understanding of NBNs toxicity, the mechanisms underlying their toxicological effects, and the strategies for mitigating associated health risks. We begin by examining the physicochemical properties of NBNs, such as particle size, composition and surface functionalization, which are key determinants of their biological interactions and toxicity. Then, through an extensive analysis of in vitro and in vivo studies, we highlight the adverse effects of NBNs exposure, including the generation of reactive oxygen species (ROS), oxidative stress, inflammation, cytotoxicity, genotoxicity, and immunotoxicity. To address the potential health risks associated with NBNs, we propose future strategies for risk prevention, including the development of safer nanomaterial designs, implementation of stringent regulatory guidelines, and advancement of novel toxicity testing approaches.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"211"},"PeriodicalIF":10.6,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of NIR photocleavable nanoparticles with BDNF for vestibular neuron regeneration.","authors":"Celine Dg Abueva, Sung Ryeong Yoon, Nathaniel T Carpena, Seung Cheol Ahn, So-Young Chang, Ji Eun Choi, Min Young Lee, Jae Yun Jung","doi":"10.1186/s12951-025-03298-x","DOIUrl":"10.1186/s12951-025-03298-x","url":null,"abstract":"<p><p>Among nanoparticle platforms, light or photoresponsive nanoparticles have emerged as a promising drug delivery strategy with spatiotemporal control while minimizing off-target effects. The characteristic absorption spectrum of the photoresponsive moiety dictates the wavelength of light needed to activate bond cleavage. However, the low tissue penetration depth limit and short-wavelength ultraviolet (UV) cellular toxicity are considered disadvantageous. This study developed a vestibular ganglion neuron organoid as a model for vestibulopathy. UV and near-infrared (NIR) radiation targeted the inner ear and neural cells, followed by toxicity evaluation. A significantly smaller toxicity of NIR light was confirmed. The photocleavage release of brain-derived neurotrophic factor (BDNF) was used by applying NIR wavelength. The results indicate that polyethylene glycol octamethylene diamine derivative conjugated with leucomethylene blue with an ethanolamine linker nanoparticle can be effectively disassembled and release BDNF when using the 808 nm laser as a trigger. The findings of the cytotoxicity assay suggest that photocleavable nanoparticles (PCNs) and laser irradiation are safe and biocompatible for human-derived and neural progenitor types of cells. Phototriggered BDNF release by NIR laser supported the growth and differentiation of human neural progenitor cells in culture. In addition, the vestibulopathy organoid exhibited a significant regenerative effect. This study harnesses the full potential of NIR laser PCNs to treat vestibular neuropathies.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"209"},"PeriodicalIF":10.6,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CREB1/CRTC2 regulated tubular epithelial-derived exosomal miR-93-3p promotes kidney injury induced by calcium oxalate via activating M1 polarization and macrophage extracellular trap formation.","authors":"Yushi Sun, Bojun Li, Baofeng Song, Yuqi Xia, Xiangjun Zhou, Fangyou Lin, Ting Rao, Fan Cheng","doi":"10.1186/s12951-025-03246-9","DOIUrl":"10.1186/s12951-025-03246-9","url":null,"abstract":"<p><strong>Background: </strong>Calcium oxalate (CaOx) crystals are known to cause renal injury and trigger inflammatory responses. However, the role of exosome-mediated epithelial-macrophage communication in CaOx-induced kidney injury remains unclear.</p><p><strong>Methods: </strong>To identify key molecules, miRNA sequencing was conducted on exosomes derived from CaOx-treated (CaOx-exo) and control (Ctrl-exo) epithelial cells, identifying miR-93-3p as significantly upregulated. A combination of dual-luciferase reporter assays, Western blot, RT-qPCR, immunofluorescence staining, flow cytometry, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation-qPCR (CHIP-qPCR) was used to explore the regulation of miR-93-3p by CREB1/CRTC2 and its downstream effects on NFAT5/Akt1/NIK/NF-κB2 signaling in macrophages. The functional roles of NFAT5 in macrophage polarization and macrophage extracellular traps (METs) formation were further evaluated both in vitro and in vivo.</p><p><strong>Results: </strong>Epithelial exosomes stimulated by CaOx crystals were found to promote kidney injury via macrophage polarization and METs formation. Treatment with NIK SMI1, a NIK inhibitor, or CI-amidine, a METs inhibitor, mitigated crystal deposition and CaOx-induced kidney damage. Overexpression of NFAT5 in a CaOx-induced mouse model reduced renal injury and crystal deposition, downregulated NIK and NF-κB2 levels, and decreased the number of M1-polarized macrophages. Mechanistic studies revealed that miR-93-3p directly targets NFAT5 mRNA, as confirmed by dual-luciferase assays, qRT-PCR, and Western blot. Additionally, we demonstrated that CREB1/CRTC2 acts as a transcriptional activator of miR-93-3p. Inhibition of miR-93-3p partially reversed NIK/NF-κB2 activation and alleviated kidney injury.</p><p><strong>Conclusions: </strong>CaOx crystals exacerbate renal interstitial injury by promoting M1 macrophage polarization and METs formation through the CREB1/CRTC2-exosomal miR-93-3p-NIK/NF-κB2 signaling pathway. Targeting this pathway may provide therapeutic avenues for mitigating crystal deposition-induced kidney damage.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"204"},"PeriodicalIF":10.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing the power of traceable system C-GAP: homologous-targeting to fire up T-cell immune responses with low-dose irradiation.","authors":"Weijie Zhuang, Kuangwu Pan, Jie Wu, Leyi Liu, Shiyu Lv, Jiajun Hu, Fangyang Shi, Wei Zhao, Dongsheng Yu","doi":"10.1186/s12951-025-03281-6","DOIUrl":"10.1186/s12951-025-03281-6","url":null,"abstract":"<p><p>While radiotherapy-induced immunogenic cell death (ICD) holds potential for enhancing cancer immunotherapy, the conventional high-dose irradiation often leads to an immunosuppressive microenvironment and systemic toxicity. Therefore, a biomimetic nanoplatform cell membrane coated-nitrogen-doped graphene quantum dots combined with Au nanoparticles (C-GAP) was developed in this study. Firstly, homologous and traceable targeting features of C-GAP enables tumor-selective accumulation, providing reference for the selection of the timing of radiotherapy. Secondly, radiosensitization by C-GAP with Low-dose irradiation (LDI) amplifies reactive oxygen species (ROS) generation to trigger potent ICD. Thirdly, remarkable immune remodeling induced by C-GAP enhances CD8⁺ T cell infiltration and effector function. Single-cell RNA sequencing revealed that C-GAP-LDI combination upregulates TNF and CCL signaling pathway expression in tumor-infiltrating CD8⁺ T cells which potentiates tumor eradication. Our findings present a novel approach for safe and effective radioimmunotherapy, where C-GAP sensitized LDI achieves therapeutic enhancement through precise ICD induction and systemic immune activation.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"207"},"PeriodicalIF":10.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage-derived mitochondria-rich extracellular vesicles aggravate bone loss in periodontitis by disrupting the mitochondrial dynamics of BMSCs.","authors":"Jiayin Yan, Tian Yang, Siyuan Ma, Danfeng Li, Cheng Hu, Jiali Tan","doi":"10.1186/s12951-025-03178-4","DOIUrl":"10.1186/s12951-025-03178-4","url":null,"abstract":"<p><strong>Background: </strong>Periodontitis is the leading cause of tooth loss in adults due to progressive bone destruction, which is closely related to the dysfunction of bone mesenchymal stem cells (BMSCs). Existing evidence suggests that mitochondrial disorders are associated with periodontitis. However, whether mitochondrial dysregulation contributes to the osteogenic impairment of BMSCs and the underlying mechanisms remain unclear. Macrophages have been shown to communicate extensively with BMSCs in periodontitis. Recent studies have reported a novel manner of cellular communication in which mitochondria-rich extracellular vesicles（MEVs） transfer mitochondria from parent cells to recipient cells, playing a role in both physiological and pathological conditions. Therefore, we aimed to investigate the role of MEVs in orchestrating the crosstalk between macrophages and BMSCs in periodontitis to formulate management strategies for bone loss.</p><p><strong>Results: </strong>Our results revealed that macrophages underwent significant mitochondrial dysfunction and inflammation in periodontitis and that MEVs derived from these macrophages played a role in alveolar bone destruction. Furthermore, cell imaging showed that inflammatory macrophages packaged numerous damaged mitochondria into MEVs, and the entry of these impaired mitochondria into BMSCs disrupted mitochondrial dynamics and hindered donut-shaped mitochondria formation, leading to osteogenic dysfunction. Proteomic analysis revealed that the proteins enriched in macrophage-derived MEVs were largely related to mitochondria and the formation and transport of vesicles. Additionally, we found that MEVs from macrophages significantly increased lipocalin 2 (LCN2) in BMSCs in periodontitis and that LCN2 perturbed mitochondrial morphological changes in BMSCs by inducing the degradation of OMA1 and accumulation of OPA1, resulting in osteogenesis impairment in BMSCs. Inhibition of LCN2 rescued the osteogenic dysfunction of BMSCs and alveolar bone loss in periodontitis.</p><p><strong>Conclusions: </strong>The transfer of mitochondria to BMSCs via MEVs exacerbates alveolar bone resorption through LCN2/OMA1/OPA1 signaling in periodontitis. Inhibition of LCN2 alleviates inflammatory bone loss, suggesting a promising therapeutic strategy for periodontitis.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"208"},"PeriodicalIF":10.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acid-responsive aggregated carrot-derived nanoantioxidants alleviate oxidative stress and restore osteoblast activity.","authors":"Jiao Peng, Rongyan Liu, Junyi Xu, Yingjuan Yao, Beibei Li, Dengke Chen, Zhuangpeng Chang, Rui Zhao, Yanlin Feng, Ruigang Hou, Min Lee, Xiao Zhang","doi":"10.1186/s12951-025-03235-y","DOIUrl":"10.1186/s12951-025-03235-y","url":null,"abstract":"<p><strong>Background: </strong>Excessive generation of reactive oxygen species is a hallmark of the osteoporotic bone microenvironment, which leads to the damage of mitochondrial function and the deactivation of osteoblasts. Fruits and vegetables are rich sources of antioxidants, which play a key role in scavenging free radicals and maintaining the body's homeostasis.</p><p><strong>Results: </strong>Herein, we have developed a type of vesicle coming from carrots as nanoantioxidants to counteract oxidative stress and restore the vitality of osteoblasts for reversing osteoporosis. Nanovesicles are derived from carrot juice using a straightforward extrusion method, resulting in stable membrane structures containing various lipids and homologous active phytochemicals. Nanovesicles can maintain stable structures under normal physiological conditions (pH 7.4) and transform into aggregates in response to the acidic extracellular pH of osteoporosis (pH 4.0). As anticipated, nanovesicles can passively target and aggregate to osteoporotic bone, ease oxidative stress, restore mitochondrial function, promote osteoblastogenesis, and reduce bone loss in osteoporotic mice.</p><p><strong>Conclusions: </strong>This work presents the first demonstration of nanovesicles derived from carrots as novel nanoantioxidants to realize the long-awaited osteogenesis, contributing to the exploration of a brand-new idea for reversing osteoporosis.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"206"},"PeriodicalIF":10.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injectable hydrogels with ROS-triggered drug release enable the co-delivery of antibacterial agent and anti-inflammatory nanoparticle for periodontitis treatment.","authors":"Yujing Zhu, Ziliang Xiu, Xiaoxi Jiang, Huifang Zhang, Xiaofeng Li, Yunru Feng, Bojiang Li, Rui Cai, Chunhui Li, Gang Tao","doi":"10.1186/s12951-025-03275-4","DOIUrl":"10.1186/s12951-025-03275-4","url":null,"abstract":"<p><p>Periodontitis, a chronic inflammatory disease caused by bacteria, is characterized by localized reactive oxygen species (ROS) accumulation, leading to an inflammatory response, which in turn leads to the destruction of periodontal supporting tissues. Therefore, antibacterial, scavenging ROS, reducing the inflammatory response, regulating periodontal microenvironment, and alleviating alveolar bone resorption are effective methods to treat periodontitis. In this study, we developed a ROS-responsive injectable hydrogel by modifying hyaluronic acid with 3-amino phenylboronic acid (PBA) and reacting it with poly(vinyl alcohol) (PVA) to form a borate bond. In addition, the ROS-responsive hydrogel encapsulated the antibacterial agent minocycline hydrochloride (MH) and Fe-Quercetin anti-inflammatory nanoparticles (Fe-Que NPs) for on-demand drug release in response to the periodontitis microenvironment. This hydrogel (HP-PVA@MH/Fe-Que) exhibited highly effective antibacterial properties. Moreover, by modulating the Nrf2/NF-κB pathway, it effectively eliminated ROS and promoted macrophage polarization to the M2 phenotype, reducing inflammation and enhancing the osteogenic differentiation potential of human periodontal ligament stem cells (hPDLSCs) in the periodontal microenvironment. Animal studies showed that HP-PVA@MH/Fe-Que significantly reduced alveolar bone loss and enhanced osteogenic factor expression by killing bacteria and inhibiting inflammation. Thus, HP-PVA@MH/Fe-Que hydrogel had efficient antibacterial, ROS-scavenging, anti-inflammatory, and alveolar bone resorption-alleviation abilities, showing excellent application potential for periodontitis healing.</p>","PeriodicalId":16383,"journal":{"name":"Journal of Nanobiotechnology","volume":"23 1","pages":"205"},"PeriodicalIF":10.6,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11900060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}