Biomaterials最新文献_第4页

Procoagulant, antibacterial and antioxidant high-strength porous hydrogel adhesives in situ formed via self-gelling hemostatic microsheets for emergency hemostasis and wound repair 通过自凝胶止血微片在原位形成的促凝、抗菌和抗氧化高强度多孔水凝胶粘合剂，用于紧急止血和伤口修复。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-30 DOI: 10.1016/j.biomaterials.2024.122936

Yingli Shan , Feng Cao , Xin Zhao , Jinlong Luo , Haoliang Mei , Limou Zhang , Ying Huang , Yutong Yang , Liangruijie Yan , Yayong Huang , Yong Han , Baolin Guo

Procoagulant, antibacterial and analgesic hemostatic hydrogel dressing with high wet tissue adhesion, ultra-high burst pressure, and easy preparation shows huge promising for rapid hemostasis in emergencies, yet it remains a challenge. Herein, we propose hemostatic microsheets based on quaternized chitosan-g-gallic acid (QCS-GA) and oxidized hyaluronic acid (OHA), which merge the benefits of sponges, hydrogels, and powders for rapid hemostasis and efficient wound healing. Specifically, they exhibit a large specific surface area and excellent hydrophilicity, rapidly absorbing blood and self-gelling through electrostatic interaction and Schiff base crosslinking. And this results in dense, porous hydrogel adhesives with superior mechanical properties, adhesion strength, and ultra-high burst pressure. Furthermore, the microsheets are biocompatible, biodegradable, and possess procoagulant, antibacterial, and antioxidant properties. In mouse and rat liver hemorrhage models, the optimized formulation (QCS-GA + OHA4) demonstrated superior hemostatic effects compared to Celox. In particular, QCS-GA + OHA4 microsheets could stop bleeding quickly from rat femoral artery transection and deliver lidocaine to provide analgesia during emergency treatment. Additionally, they promoted wound healing in mouse full-thickness skin defect wound. These easy-to-manufacture hemostatic microsheets are adaptable to irregular wounds, providing a novel solution for rapid hemostasis and wound healing.

具有高湿组织粘附性、超高爆破压和易于制备的促凝、抗菌和止痛止血水凝胶敷料在紧急情况下的快速止血方面具有巨大的前景，但这仍然是一项挑战。在此，我们提出了基于季铵盐化壳聚糖-没食子酸（QCS-GA）和氧化透明质酸（OHA）的止血微片，它融合了海绵、水凝胶和粉末的优点，可实现快速止血和高效伤口愈合。具体来说，它们具有较大的比表面积和出色的亲水性，能迅速吸收血液，并通过静电作用和希夫碱交联实现自胶化。这就形成了致密、多孔的水凝胶粘合剂，具有优异的机械性能、粘合强度和超高爆破压力。此外，这种微片还具有生物相容性、生物可降解性，以及促凝血、抗菌和抗氧化特性。在小鼠和大鼠肝脏出血模型中，优化配方（QCS-GA + OHA4）的止血效果优于 Celox。特别是，QCS-GA + OHA4 微片能迅速止住大鼠股动脉横断处的出血，并在紧急治疗期间输送利多卡因以提供镇痛。此外，它们还能促进小鼠全厚皮肤缺损伤口的愈合。这些易于制造的止血微片可适应不规则伤口，为快速止血和伤口愈合提供了一种新的解决方案。

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引用次数: 0

Reverse magnetic resonance tuning nanoplatform with heightened sensitivity for non-invasively multiscale visualizing ferroptosis-based tumor sensitization therapy 具有更高灵敏度的反向磁共振调谐纳米平台，用于无创多尺度可视化基于铁素体的肿瘤增敏疗法。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-30 DOI: 10.1016/j.biomaterials.2024.122935

Yi Zhu , Jiali Deng , Hongwei Lu , Zhu Mei , Ziwei Lu , Jiajing Guo , An Chen , Rong Cao , Xinyi Ding , Jingyi Wang , Helen Forgham , Ruirui Qiao , Zhongling Wang

Ferroptosis-based therapy has garnered considerable attention for its ability to kill drug-resistant cancer cells. Consequently, it holds great significance to assess the therapeutic outcomes by monitoring ferroptosis-related biomarkers, which enables the provision of real-time pathological insights into disease progression. Nevertheless, conventional imaging technology suffers from limitations including reduced sensitivity and difficulty in achieving real-time precise monitoring. Here, we report a tumor acidic-microenvironment-responsive nanoplatform with “Reverse Magnetic Resonance Tuning (ReMRT)” property and effective combined chemodynamic therapy (CDT) through the loading of chemotherapeutic drugs. This reverse MR mapping change is correlated with iron ion, reactive oxygen species (ROS) generation and drug release, etc., contributing to the precise monitoring of chemo-CDT effectiveness. Furthermore, the ReMRT nanoplatform presents as a highly efficacious combined chemo-CDT agent, and when this nanoplatform is used in conjunction with the “Area Reconstruction” method, it can afford a significant sensitivity (95.1-fold) in multiscale visualization of therapeutic, compared with the conventional MR R₁/R₂ values. The high-sensitive biological quantitative imaging provides a novel strategy for MR-guided multiscale dynamic tumor-related ferroptosis therapy.

基于铁蛋白沉积的疗法能够杀死耐药癌细胞，因而备受关注。因此，通过监测与铁蛋白沉积相关的生物标志物来评估治疗效果具有重要意义，因为这可以提供有关疾病进展的实时病理信息。然而，传统的成像技术存在灵敏度低、难以实现实时精确监测等局限性。在此，我们报告了一种具有 "反向磁共振调谐（ReMRT）"特性的肿瘤酸性微环境响应纳米平台，通过装载化疗药物实现了有效的化学动力学联合治疗（CDT）。这种反向磁共振图谱变化与铁离子、活性氧（ROS）生成和药物释放等相关，有助于精确监测化疗-CDT 的疗效。此外，ReMRT 纳米平台是一种高效的化疗-CDT 组合药物，当该纳米平台与 "区域重建 "方法结合使用时，与传统的磁共振 R1/R2 值相比，它在治疗的多尺度可视化方面具有显著的灵敏度（95.1 倍）。高灵敏度的生物定量成像为磁共振引导的多尺度动态肿瘤相关铁突变治疗提供了一种新策略。

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引用次数: 0

Corrigendum to 'Enhancing CAR-T cell therapy against solid tumor by drug-free triboelectric immunotherapy' [Biomaterials 314 (2025) 122871]. 通过无药三电免疫疗法增强针对实体瘤的 CAR-T 细胞疗法"[《生物材料》314 (2025) 122871] 勘误。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-30 DOI: 10.1016/j.biomaterials.2024.122927

Haimei Li, Zichen Wang, Yulin Hu, Guangqin He, Liang Huang, Yi Liu, Zhong Lin Wang, Peng Jiang

引用次数: 0

Nanoradiosentizers with X ray-actuatable supramolecular aptamer building units for programmable immunostimulatory T cell engagement 带有 X 射线可动超分子适配体构建单元的纳米放射增效剂，用于可编程免疫刺激 T 细胞参与。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-29 DOI: 10.1016/j.biomaterials.2024.122924

Jinming He , Xijiao Ren , Qiqi Zhang , Shuang Wang , Zhongjun Li , Kaiyong Cai , Menghuan Li , Yan Hu , Qian Ran , Zhong Luo

The insufficient activation and impaired effector functions of T cells in the immunosuppressive tumor microenvironment (TME) substantially reduces the immunostimulatory effects of radiotherapy. Herein, a multifunctional nanoradiosensitizer is established by integrating molecularly engineered aptamer precursors into cisplatin-loaded liposomes for enhancing radio-immunotherapy of solid tumors. Exposure to ionizing radiation (IR) following the nanoradiosensitizer treatment would induce pronounced immunogenic death (ICD) of tumor cells through cisplatin-mediated radiosensitization while also trigger the detachment of the aptamer precursors, which further self-assemble into PD-L1/PD-1-bispecific aptamer-based T cell engagers (CA) through the bridging effect of tumor-derived ATP to direct T cell binding onto tumor cells in the post-IR TME in a spatial-temporally programmable manner. The CA-mediated post-IR tumor-T cell engagement could override the immunosuppressive barriers in TME and enhance T cell-mediated recognition and elimination of tumor cells while minimizing systemic toxicities. Overall, this work offers an innovative approach to enhance the radio-immunotherapeutic efficacy in the clinics.

在具有免疫抑制作用的肿瘤微环境（TME）中，T细胞活化不足且效应功能受损，这大大降低了放射治疗的免疫刺激效果。本文通过将分子设计的aptamer前体整合到顺铂负载脂质体中，建立了一种多功能纳米放射增敏剂，用于增强实体瘤的放射免疫治疗。在纳米放射增敏剂治疗后暴露于电离辐射（IR）中，会通过顺铂介导的放射增敏作用诱导肿瘤细胞明显的免疫原性死亡（ICD），同时也会引发aptamer前体的脱落、通过肿瘤源性 ATP 的桥接效应，这些前体进一步自组装成基于 PD-L1/PD-1 双特异性适配体的 T 细胞吞噬体（CA），以空间-时间可编程的方式引导 T 细胞结合到IR 后 TME 中的肿瘤细胞上。CA介导的后IR肿瘤细胞-T细胞结合可以克服TME中的免疫抑制障碍，增强T细胞介导的肿瘤细胞识别和清除，同时最大限度地减少全身毒性。总之，这项工作为提高放射免疫治疗的临床疗效提供了一种创新方法。

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引用次数: 0

Targeted sonodynamic therapy induces tumor cell quasi-immunogenic ferroptosis and macrophage immunostimulatory autophagy in glioblastoma 靶向声动力疗法在胶质母细胞瘤中诱导肿瘤细胞准免疫性铁变态反应和巨噬细胞免疫刺激自噬作用

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-28 DOI: 10.1016/j.biomaterials.2024.122913

Meng-Fei Wang , Jie Guo , Shen-Jun Yuan , Ke Li , Quan Zhang , Hui-Mei Lei , Jia-Lin Wu , Li Zhao , Yong-Hong Xu , Xiao Chen

In this study, we demonstrated the mechanism of a glioblastoma (GBM)-targeted sonodynamic therapy (SDT) strategy employing platelets loaded with a sonosensitizer based on functionalized boron nitride nanoparticles carrying chlorin e6 (BNPD-Ce6). In the in vitro study, we first found that the BNPD-Ce6-mediated sonodynamic action (SDA) induced remarkable viability loss, DNA damage, and cell death in the GBM cells (GBCs) but not macrophages. Surprisingly, the SDA-exposed GBCs displayed a ferroptotic phenotype while the SDA-exposed macrophages underwent immuno-stimulatory autophagy and potently potentiated the SDA's toxicity to the GBCs. The ferroptotic GBCs induced by the SDA were found to be quasi-immunogenic, characterized by the emission of some alarmins such as ATP, HSP90, and CRT, but absent HMGB1, a potent endogenous adjuvant. As such, the SDA-stressed GBCs were unable to stimulate the BMDMs. This defect, interestingly, could be rescued by platelets as a donor of HMGB1 which markedly enhanced the BNPD-Ce6's sonotoxicity to the GBCs. In the in vivo study, we first employed BNPD-Ce6-loaded platelets to achieve ultrasound-triggered, targeted delivery of BNPD-Ce6 in grafted intra-cranial GBMs and subsequent sonodynamic tumor damage. An SDT regimen designed based on these results slowed the growth of grafted intra-cranial GBMs and significantly increased the survival of the host animals. Pathological examination of the SDT-treated GBMs revealed tissue necrosis and destruction and validated the in vitro observations. Finally, the depletion of macrophages was found to abrogate the efficacy of the SDT in subcutaneous GBC grafts. In conclusion, the BNPD-Ce6@Plt-mediated SDT is a practicable and efficacious anti-GBM therapy. Its therapeutic mechanism critically involves a synergy of tumor cell ferroptosis, macrophage stimulation, and platelet activation induced by the SDA.

在这项研究中，我们展示了一种胶质母细胞瘤（GBM）靶向声动力疗法（SDT）策略的机制，该策略采用了装载有基于携带氯素e6的功能化氮化硼纳米颗粒（BNPD-Ce6）的声敏化剂的血小板。在体外研究中，我们首先发现 BNPD-Ce6 介导的声动力作用（SDA）会导致 GBM 细胞（GBCs）显著丧失活力、DNA 损伤和细胞死亡，但不会导致巨噬细胞死亡。令人惊讶的是，暴露于 SDA 的 GBC 显示出一种铁凋亡表型，而暴露于 SDA 的巨噬细胞则发生免疫刺激性自噬，并有效增强了 SDA 对 GBC 的毒性。研究发现，SDA 诱导的铁变态反应 GBC 具有准免疫原性，其特征是释放出一些警报素，如 ATP、HSP90 和 CRT，但不释放 HMGB1，而 HMGB1 是一种有效的内源性佐剂。因此，SDA 应激的 GBCs 无法刺激 BMDMs。有趣的是，这种缺陷可以通过血小板作为 HMGB1 的供体来弥补，血小板可以显著增强 BNPD-Ce6 对 GBCs 的声毒性。在体内研究中，我们首先采用了装载 BNPD-Ce6 的血小板，在超声触发下实现了 BNPD-Ce6 在颅内 GBM 移植中的靶向递送，以及随后的声动力肿瘤损伤。根据这些结果设计的 SDT 方案减缓了移植颅内 GBM 的生长，并显著提高了宿主动物的存活率。对经 SDT 处理的 GBM 进行的病理学检查显示了组织坏死和破坏，验证了体外观察结果。最后，在皮下 GBC 移植物中发现巨噬细胞的耗竭会削弱 SDT 的疗效。总之，BNPD-Ce6@Plt 介导的 SDT 是一种可行且有效的抗 GBM 疗法。它的治疗机制主要涉及 SDA 诱导的肿瘤细胞铁突变、巨噬细胞刺激和血小板活化的协同作用。

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引用次数: 0

Nanoparticle-mediated Klotho gene therapy prevents acute kidney injury to chronic kidney disease transition through regulating PPARα signaling in renal tubular epithelial cells 纳米粒子介导的 Klotho 基因疗法通过调节肾小管上皮细胞中的 PPARα 信号，防止急性肾损伤向慢性肾病转变。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-28 DOI: 10.1016/j.biomaterials.2024.122926

Hongyu Li , Yuying Ouyang , Haoran Lv , Hanzhi Liang , Siweier Luo , Yating Zhang , Haiping Mao , Tianfeng Chen , Wei Chen , Yiming Zhou , Qinghua Liu

Klotho is an anti-aging protein produced primarily by tubular epithelial cells (TECs). Down-regulated expression of Klotho in injured TECs plays a key pathogenic role in promoting acute kidney injury (AKI) to chronic kidney disease (CKD) transition, yet therapeutic approaches targeting the restoration of renal Klotho levels remain challenging for clinical application. Here, we synthesize polydopamine-polyethylenimine-l-serine-Klotho plasmid nanoparticles (PPSK NPs), which can safely and selectively deliver the Klotho gene to the injured TECs through binding kidney injury molecule-1 and maintain the expression of Klotho protein. In vitro, PPSK NPs effectively reduce the hypoxia-reoxygenation-induced reactive oxygen species production and fibrotic gene expression. In the unilateral ischemia-reperfusion injury- and folic acid-induced AKI-CKD transition mouse models, a single low-dose injection of PPSK NPs is sufficient to preserve the normal kidney architecture and prevent renal fibrosis. Mechanismly, the protective effect of PPSK NPs relies on upregulating a key molecule peroxisome proliferator-activated receptor alpha (PPARα) via the inhibition of p38 and JNK phosphorylation, which in turn improves tubular fatty acid beta-oxidation and reduces renal lipid accumulation, thereby protecting against kidney fibrosis. In conclusion, our results highlight the translational potential of nanoparticle-based Klotho gene therapy in preventing the AKI-CKD transition.

Klotho是一种抗衰老蛋白，主要由肾小管上皮细胞（TEC）产生。在急性肾损伤（AKI）向慢性肾病（CKD）转变的过程中，受伤的肾小管上皮细胞中 Klotho 的表达下调起着关键的致病作用，然而针对恢复肾小管上皮细胞 Klotho 水平的治疗方法在临床应用中仍面临挑战。在这里，我们合成了聚多巴胺-聚乙烯亚胺-丝氨酸-Klotho质粒纳米颗粒（PPSK NPs），它能通过结合肾损伤分子-1将Klotho基因安全、选择性地传递到损伤的TECs，并维持Klotho蛋白的表达。在体外，PPSK NPs 能有效减少缺氧-复氧诱导的活性氧生成和纤维化基因表达。在单侧缺血再灌注损伤和叶酸诱导的 AKI-CKD 转换小鼠模型中，单次低剂量注射 PPSK NPs 就足以保护正常的肾脏结构并防止肾脏纤维化。从机制上看，PPSK NPs 的保护作用依赖于通过抑制 p38 和 JNK 磷酸化上调关键分子过氧化物酶体增殖激活受体α（PPARα），进而改善肾小管脂肪酸 beta 氧化，减少肾脏脂质积累，从而防止肾脏纤维化。总之，我们的研究结果凸显了基于纳米粒子的 Klotho 基因疗法在预防 AKI-CKD 转化方面的转化潜力。

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引用次数: 0

Enhanced tumor-targeting ability of transferrin-functionalized magnetic nanoparticles by in vivo AMF stimulation 通过体内AMF刺激增强转铁蛋白功能化磁性纳米粒子的肿瘤靶向能力

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-28 DOI: 10.1016/j.biomaterials.2024.122925

Tingbin Zhang , Jia Li , Junjie Lu , Jianwei Li , Huan Zhang , Yuqing Miao , Xiaoli Liu , Yuan He , Lei Yang , Haiming Fan

The protein corona formed on the surface of ligand-functionalized nanoparticles has been associated with the loss of targeting capability of the nanoparticles in vivo. Here, we developed a remote magnetothermal stimulation approach to regulate the in vivo active-targeting capability of transferrin (Tf)-functionalized magnetic nanoparticles (SPIO-Tf). This technique harnesses the heat dissipation by the magnetic nanoparticles in response to alternating magnetic fields to re-expose buried Tf on the nanoparticle surface, thereby restoring its binding function. SPIO-Tf with different grafting densities were prepared and in vitro experiments reveal that AMF stimulation of SPIO-Tf significantly improved its targeting ability to A549 cells in serum-rich environments. In vivo experiments also exhibit a 2.68-fold greater accumulation of magnetothermal-stimulated SPIO-Tf in solid tumors. Moreover, our approach is applicable to various SPIO-Tf formulations with different PEG molecular weights, and antibodies-conjugated SPIO. Overall, this study establishes a versatile, safe and potent strategy to tackle the negative impact of protein corona on the targeting ability of ligand-decorated magnetic nanoparticles in vivo, with promising implications for enhancing the effectiveness of diagnostic and therapeutic interventions across a range of diseases.

配体功能化纳米粒子表面形成的蛋白电晕与纳米粒子在体内失去靶向能力有关。在这里，我们开发了一种远程磁热刺激方法来调节转铁蛋白（Tf）功能化磁性纳米粒子（SPIO-Tf）的体内活性靶向能力。该技术利用磁性纳米粒子在交变磁场作用下的散热来重新暴露纳米粒子表面埋藏的转铁蛋白，从而恢复其结合功能。我们制备了不同接枝密度的 SPIO-Tf，体外实验显示，在血清丰富的环境中，AMF 对 SPIO-Tf 的刺激显著提高了其对 A549 细胞的靶向能力。体内实验也显示，磁热刺激的 SPIO-Tf 在实体瘤中的累积量增加了 2.68 倍。此外，我们的方法还适用于不同 PEG 分子量的 SPIO-Tf 制剂和抗体结合的 SPIO。总之，这项研究建立了一种多功能、安全且有效的策略，以解决蛋白质电晕对配体装饰的磁性纳米粒子在体内靶向能力的负面影响，这对提高各种疾病的诊断和治疗干预效果具有重要意义。

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引用次数: 0

Rescue of mitochondrial dysfunction through alteration of extracellular matrix composition in barth syndrome cardiac fibroblasts 通过改变巴氏综合征心脏成纤维细胞的细胞外基质组成来挽救线粒体功能障碍。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-26 DOI: 10.1016/j.biomaterials.2024.122922

Janny Piñeiro-Llanes , Silveli Suzuki-Hatano , Ananya Jain , Sree Venigalla , Manasi Kamat , Kari B. Basso , William T. Cade , Chelsey S. Simmons , Christina A. Pacak

Fibroblast-ECM (dys)regulation is associated with a plethora of diseases. The ECM acts as a reservoir of inflammatory factors and cytokines that mediate molecular mechanisms within cardiac cell populations. The role of ECM-mitochondria crosstalk in the development and progression of cardiac disorders remains uncertain. We evaluated the influence of ECM produced by stromal cells from patients with the mitochondrial cardiomyopathy (Barth syndrome, BTHS) and unaffected healthy controls on cardiac fibroblast (CF) metabolic function. To do this, cell-derived matrices CDMs were generated from BTHS and healthy human pluripotent stem cell-derived CFs (hPSC-CF) and used as cell culture substrates. BTHS CDMs negatively impacted the mitochondrial function of healthy hPSC-CFs while healthy CDMs improved mitochondrial function in BTHS hPSC-CFs. Mass spectrometry comparisons identified 5 matrisome proteins differentially expressed in BTHS compared to healthy CDM. Our results highlight a key role for the ECM in disease through its impact on mitochondrial function.

成纤维细胞-ECM（失调）与多种疾病相关。ECM 是炎症因子和细胞因子的储存库，可介导心脏细胞群内的分子机制。ECM 与线粒体之间的相互作用在心脏疾病的发生和发展中的作用仍不确定。我们评估了线粒体心肌病（巴特综合征，BTHS）患者和未受影响的健康对照组的基质细胞产生的 ECM 对心脏成纤维细胞（CF）代谢功能的影响。为此，从 BTHS 和健康人多能干细胞衍生的成纤维细胞（hPSC-CF）中生成了细胞衍生基质 CDMs，并将其用作细胞培养基质。BTHS CDMs 对健康 hPSC-CFs 的线粒体功能产生了负面影响，而健康 CDMs 则改善了 BTHS hPSC-CFs 的线粒体功能。质谱比较发现，与健康 CDM 相比，5 种 matrisome 蛋白在 BTHS 中表达不同。我们的研究结果凸显了 ECM 通过影响线粒体功能在疾病中的关键作用。

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引用次数: 0

VEGF-loaded ROS-responsive nanodots improve the structure and function of sciatic nerve lesions in type II diabetic peripheral neuropathy 血管内皮生长因子负载的 ROS 响应纳米点可改善 II 型糖尿病周围神经病变坐骨神经病变的结构和功能。

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-26 DOI: 10.1016/j.biomaterials.2024.122906

Xiaolan Ou , Ze Wang , Daojiang Yu , Wenlai Guo , Andrei V. Zvyagin , Quan Lin , Wenrui Qu

Diabetic peripheral neuropathy (DPN) is a prevalent complication of diabetes mellitus (DM), significantly contributing to the risk of amputation and mortality. Reactive oxygen species (ROS) can induce both neurological and structural harm through direct impact and pyroptosis, underscoring the critical role of ROS regulation in mitigating DPN. In this research endeavor, we propose harnessing the inherent antioxidant properties of sulfhydryl groups by grafting them onto gold nanodots through an amidation reaction, resulting in the creation of ROS-responsive AuNDs. Additionally, we aim to synthesize AuNDs-VEGF, wherein VEGF is attached to AuNDs via electrostatic interactions, as a therapeutic strategy for addressing DPN in rat models. The results of in vivo experiments showed that AuNDs and AuNDs-VEGF nanoparticles could increase the nerve conduction velocity, shorten the latency of nerve conduction in the sciatic nerve, promote the regeneration of nerve trophectodermal vessels, improve the structure and function of the sciatic nerve, reduce the apoptosis of neural cells, and alleviate the atrophy of the gastrocnemius muscle. Thus, VEGF-loaded ROS-responsive nanodots present a promising avenue for ameliorating diabetic peripheral neuropathy. This innovative approach not only extends the application possibilities of nanodots but also introduces a novel avenue for the treatment of diabetic neuropathy.

糖尿病周围神经病变（DPN）是糖尿病（DM）的一种常见并发症，极大地增加了截肢和死亡的风险。活性氧（ROS）可通过直接撞击和热跃迁诱发神经和结构损伤，这凸显了调节 ROS 在减轻 DPN 病变中的关键作用。在这项研究工作中，我们建议利用巯基固有的抗氧化特性，通过酰胺化反应将其接枝到纳米金点上，从而创造出具有 ROS 响应性的 AuNDs。此外，我们还致力于合成 AuNDs-VEGF，通过静电相互作用将 VEGF 附着在 AuNDs 上，作为治疗大鼠模型 DPN 的策略。体内实验结果表明，AuNDs 和 AuNDs-VEGF 纳米颗粒能提高神经传导速度，缩短坐骨神经的神经传导潜伏期，促进神经滋养血管的再生，改善坐骨神经的结构和功能，减少神经细胞的凋亡，缓解腓肠肌的萎缩。因此，血管内皮生长因子负载的 ROS 响应纳米点为改善糖尿病周围神经病变提供了一条前景广阔的途径。这种创新方法不仅扩展了纳米点的应用范围，还为治疗糖尿病神经病变开辟了一条新途径。

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引用次数: 0

Bioactive mesoporous silica materials-assisted cancer immunotherapy 生物活性介孔二氧化硅材料辅助癌症免疫疗法

IF 12.8 1区医学 Q1 ENGINEERING, BIOMEDICAL

Biomaterials

Pub Date : 2024-10-25 DOI: 10.1016/j.biomaterials.2024.122919

Jiali Liu , Jiying Liu , Yaxin Wang , Fangman Chen , Yan He , Xiaochun Xie , Yiling Zhong , Chao Yang

Immunotherapy is initially envisioned as a powerful approach to train immune cells within the tumor microenvironment (TME) and lymphoid tissues to elicit strong anti-tumor responses. However, clinical cancer immunotherapy still faces challenges, such as limited immunogenicity and insufficient immune response. Leveraging the advantages of mesoporous silica (MS) materials in controllable drug and immunomodulator release, recent efforts have focused on engineering MS with intrinsic immunoregulatory functions to promote robust, systemic, and safe anti-tumor responses. This review discusses advances in bioactive MS materials that address the challenges of immunotherapy. Beyond their role in on-demand delivery and drug release in response to the TME, we highlight the intrinsic functions of bioactive MS in orchestrating localized immune responses by inducing immunogenic cell death in tumor cells, modulating immune cell activity, and facilitating tumor-immune cell interactions. Additionally, we emphasize the advantages of bioactive MS in recruiting and activating immune cells within lymphoid tissues to initiate anti-tumor vaccination. The review also covers the challenges of MS-assisted immunotherapy, potential solutions, and future outlooks. With a deeper understanding of material-bio interactions, the rational design of MS with sophisticated bioactivities and controllable responsiveness holds great promise for enhancing the outcomes of personalized immunotherapy.

免疫疗法最初被认为是训练肿瘤微环境（TME）和淋巴组织中的免疫细胞以引起强烈抗肿瘤反应的一种强有力的方法。然而，临床癌症免疫疗法仍面临着免疫原性有限和免疫反应不足等挑战。利用介孔二氧化硅（MS）材料在可控药物和免疫调节剂释放方面的优势，最近的研究重点是设计具有内在免疫调节功能的介孔二氧化硅，以促进稳健、系统和安全的抗肿瘤反应。本综述将讨论生物活性 MS 材料在应对免疫疗法挑战方面取得的进展。除了在按需递送和释放药物以应对肿瘤组织和器官方面的作用外，我们还强调了生物活性 MS 在通过诱导肿瘤细胞免疫原性细胞死亡、调节免疫细胞活性和促进肿瘤免疫细胞相互作用来协调局部免疫反应方面的内在功能。此外，我们还强调了生物活性 MS 在招募和激活淋巴组织内的免疫细胞以启动抗肿瘤疫苗接种方面的优势。综述还涵盖了 MS 辅助免疫疗法面临的挑战、潜在的解决方案以及未来展望。随着对材料-生物相互作用的深入了解，合理设计具有复杂生物活性和可控响应性的 MS 将为提高个性化免疫疗法的效果带来巨大希望。

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引用次数: 0