JOURNAL OF NANOBIOTECHNOLOGY
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2025
·Vol. 23
·期 1
·1-21
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IF 12.6
Wang Qiuyang,Feng Kai,Wan Guangsheng,Liao Wei,Jin Jing,Wang Peng,Sun Xiaolian,Wang Weijun,Jiang Qing
RNA interference (RNAi) and oxidative stress inhibition therapeutic strategies have been extensively utilized in the treatment of osteoarthritis (OA), the most prevalent degenerative joint disease. However, the synergistic effects of these approaches on attenuating OA progression remain largely unexplored. In this study, matrix metalloproteinase-13 siRNA (siMMP-13) was incorporated onto polyethylenimine (PEI)-polyethylene glycol (PEG) modified Fe3O4 nanoparticles, forming a nucleic acid nanocarrier termed si-Fe NPs. Subsequently, a poly(vinyl alcohol) (PVA) crosslinked phenylboronic acid (PBA)-modified hyaluronic acid (HA) hydrogel (HPP) was used to encapsulate the si-Fe NPs, resulting in a bifunctional hydrogel (si-Fe-HPP) with reactive oxygen species (ROS)-responsive and RNAi therapeutic properties. Studies in vitro demonstrated that si-Fe-HPP exhibited excellent biocompatibility, anti-inflammatory effects and prolonged stable retention time in knee joint. Intra-articular injection of si-Fe-HPP significantly attenuated cartilage degradation in mice with destabilization of the medial meniscus (DMM)-induced OA. The si-Fe-HPP treatment not only notably alleviated synovitis, osteophyte formation and subchondral bone sclerosis, but also markedly improved physical activity and reduced pain in DMM-induced OA mice. This study reveals that si-Fe-HPP, with its ROS-responsive and RNAi abilities, can significantly protect chondrocytes and attenuate OA progression, providing novel insights and directions for the development of therapeutic materials for OA treatment.Graphical
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Small
·
2024
·
IF 13
Qin Zhang,Weikai Chen,Guangfeng Li,Zhixin Ma,Mengru Zhu,Qianmin Gao,Ke Xu,Xinru Liu,Wenyi Lu,Wencai Zhang,Yan Wu,Zhongmin Shi,Jiacan Su
In view of the increased levels of reactive oxygen species (ROS) that disturb the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), the repair of diabetic bone defects remains a great challenge. Herein, a factor-free hydrogel is reported with ROS scavenging and responsive degradation properties for enhanced diabetic bone healing. These hydrogels contain ROS-cleavable thioketal (TK) linkers and ultraviolet (UV)-responsive norbornene (NB) groups conjugated with 8-arm PEG macromers, which are formed via UV crosslinking-mediated gelation. Upon reacting with high levels of ROS in the bone defect microenvironment, ROS-cleavable TK linkers are destroyed, allowing the responsive degradation of hydrogels, which promotes the migration of BMSCs. Moreover, ROS levels are reduced through hydrogel-mediated ROS scavenging to reverse BMSC differentiation from adipogenic to osteogenic phenotype. As such, a favorable microenvironment is created after simultaneous ROS scavenging and hydrogel degradation, leading to the effective repair of bone defects in diabetic mouse models, even without the addition of growth factors. Thus, this study presents a responsive hydrogel platform that regulates ROS scavenging and stromal degradation in bone engineering.
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BIOMACROMOLECULES
·
2024
·
IF 5.5
Wali Muhammad,Min Liang,Beiduo Wang,Jieqi Xie,Wajiha Ahmed,Changyou Gao
N-Acetyl cysteine (NAC) is an essential molecule that boosts acute lung injury (ALI) defense via its direct antioxidant capability. Nevertheless, the therapeutic use of NAC is limited due to its poor bioavailability and short half-life. In this study, NAC was grafted to the polyurethane consisting of poly(propylene fumarate), poly(thioketal), and 1,6-hexamethylene diisocyanate (PFTU) to reduce excessive oxidative stress and inflammatory factors in ALI. The NAC-grafted polymer nanoparticles (NPT@NPs) were prepared as a drug delivery system, which could effectively scavenge free radicals and reduce inflammation in vitro. The administration of NPT@NPs exhibited notable efficacy in ameliorating pulmonary edema, attenuating the presence of inflammatory cells, suppressing myeloperoxidase expression, diminishing the levels of pro-inflammatory cytokines, and reversing cell apoptosis in an ALI model induced by lipopolysaccharide (LPS). The NPT@NPs demonstrated significantly better efficacy compared to the free NAC in mitigating the deleterious effects of LPS on pulmonary tissue, thereby providing more effective protection against pulmonary inflammation.
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Small Methods
·
2024
·
IF 10.7
Weitong Hu,Shuhan Shi,Yihua Xu,Yunting Zhang,Jingyi Hu,Qiong Bian,Xiaolu Ma,Yuxian Ye,Shengfei Yang,Xiaoxia Sheng,Guang Liang,Tianyuan Zhang,Haibin Wu,Jianqing Gao
Androgenetic alopecia (AGA) is a prevalent issue affecting the physical and mental health of individuals but with fewer current treatments. Platinum nanozymes (PtNZs) are known for their excellent ability to reduce and modulate the high oxidative stress environment in AGA pathology. And microneedles are used to overcome the skin barrier due to the poor permeability of PtNZs. Herein, dissolving microneedles loaded with PtNZs (Pt-MNs) are designed and successfully induced hair regeneration in the AGA model. Pt-MNs possessed adequate mechanical strength to breach the skin barrier for effective PtNZs delivery. In vivo, PtNZs first reduced reactive oxygen species (ROS) to oxygen, which recovered the AGA pathological environment. And the oxygen then increased oxidative phosphorylation, promoting the differentiation of hair follicle stem cells to achieve hair regeneration. The group treated with Pt-MNs with a dosing frequency of once every three days achieved faster hair growth than the daily application of the positive drug minoxidil. Further safety experiments showed that the application of Pt-MNs locally opened temporary and recoverable skin channels, with no retention of Pt in major organs, indicating high safety. In conclusion, this study indicated the potential of Pt-MNs as an effective method for treating AGA.
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CHEMICAL ENGINEERING JOURNAL
·
2024
·
IF 13.3
Ziyang Liu,Jing Mao,Weiqi Li,Chenci Xu,An Lao,Airi Shin,Jiaqing Wu,Anqi Gu,Zhen Zhang,Lixia Mao,Kaili Lin,Jiaqiang Liu
Diabetic patients often suffer from delayed tissue healing and bone metabolism disorder, presenting a significant clinical challenge in the regeneration of diabetic bone defects. Hyperglycemia weakens osteogenesis and angiogenesis and destroys the balance of homeostasis. To solve this problem, a smart glucose-sensitivity sustained-release Resveratrol-loaded hydrogel platform is proposed to restore the function of mesenchymal stem cells. In this study, phenylboronic acid (PBA), known for its unique glucose sensitivity, is grafted onto the methacrylated gelatin (GelMA) chain, enabling the immobilization of Resveratrol (Res) molecules within the hybrid hydrogel through dynamic borate bond formation. Both in vivo and in vitro findings demonstrate that this hydrogel platform effectively scavenges excessive reactive oxygen species, ameliorates inflammation, modulates macrophage polarization, and enhances osteogenesis by activating the PI3K/AKT/GSK-3β signaling pathway. Collectively, all results suggest that this novel glucose-responsive hydrogel platform may be a potential therapy for diabetic bone regeneration.
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Small
·
2024
·Vol. 20
·期 52
·2407802
·
IF 13
Mengyang Li,Yuhang Dong,Yage Shang,Jiaqi Liu,Yunchuan Wang,Dongliang Zhang,Lixia Zhang,Chao Han,Yue Zhang,Kuo Shen,Yaoxiang Yang,Hongtao Wang,Hao Guan,Dahai Hu
Excessive generation of reactive oxygen species (ROS) poses a huge obstacle to the healing process of diabetic wounds, resulting in chronic, non-healing wounds. While numerous anti-ROS therapeutics have been developed, satisfied intra- and extra- cellular ROS homeostasis is hard to be established in diabetic wounds. To address this issue, a nanoparticle via loading metformin and CeO 2 into mesoporous silica (MSN@Met-CeO 2 ) is designed and synthesized, which is then encapsulated within ROS-responsive hydrogel and shaped as microneedles (MNs) for better application in diabetic wounds. Interestingly, a unique metformin-cerium chelate (Ce· 3Metformin) is formed during the synthesis of MSN@Met-CeO 2 MN, which significantly strengthened the inhibitory effect of metformin on mitochondrial complex I. With the presence of Ce· 3Metformin, MSN@Met-CeO 2 MN performed a remarkable effect on intracellular mtROS reduction as well as extracellular ROS elimination, the latter is primarily accomplished through the dissociative CeO 2 in MSN@Met-CeO 2 MN. In the mouse diabetic wound model, MSN@Met-CeO 2 MN exhibited a superior pro-healing effect with accelerated inflammation resolution and enhanced angiogenesis, thus highlighting its significant potential for clinical application
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ACS Biomaterials Science & Engineering
·
2024
·
IF 5.4
Wajiha Ahmed,Shifen Li,Min Liang,Yongyuan Kang,Xiaoqing Liu,Changyou Gao
Elevated levels of ROS, bacterial infection, inflammation, and improper regeneration are the factors that need to be addressed simultaneously for achieving effective wound healing without scar formation. This study focuses on the fabrication of electrospun ROS-responsive selenium-containing polyurethane nanofibers incorporating deferoxamine mesylate (Def), indomethacin (Indo), and gold nanorods (AuNRs) as proangiogenesis, anti-inflammatory, and antibacterial agents for synchronized delivery to a full-thickness wound in vivo. The structure of the fabricated nanofibers was analyzed by various techniques. Toxicity was checked by CCK-8 and hemolytic assays. The efficiency of wound healing in vitro was verified by a transwell assay and cell scratch assay. The wound healing efficiency of the nanofibers was assayed in full-thickness wounds in a rat model. The multifunctional nanofibers had a porous structure, enhanced antioxidation, antibacterial activity, and promoted wound healing. They eradicated TNF-α and IL-6, increased IL-10 expression, and revealed the angiogenic potential by increased expression of HIF-1α, VEGF, and CD31.
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FISH & SHELLFISH IMMUNOLOGY
·
2025
·
IF 3.9
Mijia Li,Wei Yuan,Shiyi Duan,Yang Li,Sijie Zhang,Yan Zhao,Shimei Xiao,Keyuan Zhong
The large-scale mining and utilization of rare earth elements have significantly increased their concentration in the environment, especially in regions surrounding mining areas. These environmentally-enriched rare earth elements accumulate in agricultural products and organisms through soil and water, potentially impacting in human health through the food chain. Erbium (Er), a rare earth element of the lanthanide series (Group IIIB), plays a crucial role in various modern technological applications. It is primarily utilized in ceramics, glass coloring, optical fibers, laser technology, and the nuclear industry, among others. However, a paucity of information on the health effects and ecotoxicity of erbium is currently available. In this study, we used the zebrafish as experimental animal to investigate the potential impact of the rare earth element erbium on the immune system. We exposed fertilized zebrafish embryos to different concentrations of erbium (0, 4, 8 and 16 mg/L) from 6 hours post-fertilization (hpf) until 72 hpf. We found that with increasing concentrations of erbium exposure, there was an increasing and dispersing trend in the number of zebrafish neutrophils; a decreasing trend in the number of macrophages. Exposure to erbium was demonstrated to impair the phagocytic capability of macrophages, reduce the recruitment of neutrophils to the wound site, and lower the resistance of zebrafish to Escherichia coli infection. Erbium exposure led to macrophage apoptosis and upregulation of oxidative stress in the zebrafish. The individual application of the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine, the IKBKB inhibitor resveratrol and the NF-κB inhibitor andrographolide was demonstrated to alleviate erbium-induced immune toxicity, as confirmed by assays including acridine orange staining, neutrophil enumeration and recruitment, and real-time quantitative PCR. Therefore, the rare earth element erbium induced immune toxicity in zebrafish through the ROS/NF-κB pathway. The findings of this study provide information for assessing the impact of rare earth elements on human health and ecosystems.
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Materials Today Bio
·
2025
·
IF 10.2
Shaoyin Wei,Dong Yang,Zeyu Shou,Yipiao Zhang,Shengwu Zheng,Xingjie Zan,Lianxin Li,Chunwu Zhang
Defective diabetic wound healing is a major clinical challenge, where hyperglycemia at the wound site induces excessive reactive oxygen species (ROS) which activate the MAPK pathway (particularly p38 MAPK), resulting in sustained release of inflammatory factors and cellular damage/apoptosis. Polyphenols are efficient ROS scavengers which reduce the level of inflammation at the wound site and promote wound healing, but the low bioavailability limits their biomedical application. This study developed a simple and highly efficient method for preparing proanthocyanidin (PC) capsules through hydrogen bonding and hydrophobic interactions among PC molecules. PC capsules can continuously scavenge free radicals and release proanthocyanidins, significantly enhancing their bioavailability. A single dose of PC capsules accelerates wound healing in diabetic mice by regulating the p38 MAPK signaling cascade, reducing inflammatory mediator concentration, inhibiting cell apoptosis, and remodeling the wound microenvironment. This research makes an important contribution to the field of enhancing polyphenol bioavailability for wound healing and reveals the potential of modulating the MAPK pathway for treating other inflammation and oxidative stress-related diseases.
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Materials Today Bio
·
2024
·
IF 8.7
Linxiao Sun,Shaoyin Wei,Chenglong Wang,Yipiao Zhang,Xingjie Zan,Lianxin Li,Chunwu Zhang
Chronic inflammatory diseases such as diabetic wounds and osteoarthritis are significant threats to human health. Failure to scavenge longstanding excessive reactive oxygen species (ROS) is an important cause of chronic inflammatory diseases, yet existing treatments that provide long-lasting therapeutic effects are limited. Here, procyanidin capsules were synthesized in a simple one-step way using calcium carbonate as a template. The biosafety of procyanidin capsules in vitro and in vivo was monitored by cytotoxicity and pathological sections. The therapeutic effect of procyanidin capsules in diabetic wounds and osteoarthritis was accessed by pathological evaluation combined with the quantification of inflammatory markers. The data showed that procyanidin capsules could long-term scavenge excessive ROS and effectively promote articular cartilage repair in osteoarthritis, accelerating diabetic wound healing. Lastly, transcriptome analysis suggested that procyanidin capsules commonly regulated adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling in diabetic wounds and osteoarthritis. This study provides a straightforward protocol for creating procyanidin capsules, while presenting a promising new therapeutic option for long-term scavenging ROS in chronic inflammatory diseases.
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JOURNAL OF CONTROLLED RELEASE
·
2025
·
IF 11.5
Yuling Chen,Na Yin,Shenyao Jin,Liya Yang,Yanyun He,Ling Guo,Min Feng
Osteoarthritis is the most prevalent form of arthritis, and a leading cause of pain and long-term disability. Dysregulation of redox homeostasis is a key feature in the pathological progression of osteoarthritis that amplifies the inflammatory response, aggravates synovitis and accelerates cartilage degradation. Herein, a hemin and chitosan-mediated antioxidant gel inducing ROS conversion (hc-MAGIC) was constructed to targeting oxidative stress for osteoarthritis treatment. The optimized hc-MAGIC exhibited autonomous sol-gel-sol transition properties, which enable to be administered via intra-articular injections, prolong retention in the joint cavity, and controlled modulation of inflammation in response to ROS. Notably, with extracellular ROS fueled, hc-MAGIC could address hypoxia in the osteoarthritic joint cavity through spatiotemporally controlled generation of oxygen (O 2 ). Moreover, hc-MAGIC restored the impaired antioxidative capacity of macrophages by upregulating HO-1 on demand, resulting in suppressing excessive intracellular ROS generation. Consequently, by restoring both extracellular and intracellular redox homeostasis in osteoarthritic joints, hc-MAGIC markedly reversed the inflammatory microenvironment to support chondrogenesis, prevented cartilage degradation, and promoted cartilage repair by augmenting cartilage matrix formation. Therefore, featuring its sol-gel-sol transition properties，ROS-to-O 2 conversion, and dual-mode redox regulation, hc-MAGIC offers a potent novel therapy for on-demand modulation of inflammation in osteoarthritis.
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MOLECULAR NEUROBIOLOGY
·
2025
·
IF 4.3
Li Xinying,Li Weiran,Xie Xinying,Fang Ting,Yang Jingwen,Shen Yue,Wang Yicheng,Wang Hongyan,Tao Liqing,Zhang Heng
Rotenone, a plant-derived natural insecticide, is widely used to induce Parkinson’s disease (PD) models. However, the mechanisms of rotenone-induced cell death remain unclear. Here, we found that rotenone (0.01, 0.1, or 1 μmol/L) suppressed SH-SY5Y dopamine neuron viability and led to PD-like pathological changes, such as reduced tyrosine hydroxylase (TH) but increased α-synuclein. Rotenone increased the levels of intracellular reactive oxygen species (ROS) and mitochondrial ROS, as well as the levels of the antioxidants nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), ultimately resulting in oxidative stress. Moreover, rotenone significantly downregulated the expression of GPX4 and xCT but upregulated the expression of COX2 and NCOA4, which are markers of ferroptosis. Furthermore, rotenone decreased phosphorylated mTOR level but increased Beclin-1, ATG5, LC3 and p62 expression, suggesting that rotenone enhances autophagy and reduces autophagy flux. Additionally, rotenone reduced Bcl-2 levels and the mitochondrial membrane potential (MMP) while promoting BAX and Caspase-3 expression, thus initiating cell apoptosis. N-acetylcysteine (NAC), a ROS scavenger, and ferrostatin-1 (Fer-1) and deferoxamine (DFO), two ferroptosis inhibitors, significantly eliminated rotenone-induced autophagy and apoptosis. Moreover, ML385, a specific inhibitor of Nrf2, suppressed rotenone-induced ferroptosis. Our results demonstrated that ROS might mediate rotenone-induced PD-like pathological changes by regulating iron death, autophagy, and apoptosis. Inhibiting ferroptosis blocked the rotenone-induced increase in autophagy and apoptosis. Thus, the ability of ROS to regulate rotenone-induced death through autophagy and apoptosis is dependent on ferroptosis. The findings require validation in multiple neuronal cell lines and in vivo.
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