INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
·
IF 7.7
Dong-Xu Tang,Kun Liu,Jin-Yu Yang,Zhi-Jun Wang,Li-Li Fu,Xiao-Jie Yang,Yue-Sheng Li,Bin Huang,Yi Liu
The process of diabetic wound healing was influenced by the excessive proliferation of reactive oxygen species (ROS). Therefore, in the process of healing diabetic wounds, it was crucial to removing ROS. This study designed composited nanoparticles: KBP, consisted by Konjac glucomannan, bovine serum albumin, and Prussian blue. Then they were embedded in Konjac glucomannan and hydroxypropyl trimethylammonium chloride chitosan composite hydrogel (KH), The KBP@KH hydrogel finally achieved excellent efficacy in diabetic wound healing. The in vitro and in vivo experiments demonstrated that KPB nanoparticles exhibited favorable ROS scavenging capability and biosafety. The KBP@KH hydrogel not only effectively eliminated ROS from diabetic wounds, but also exhibited excellent wound adaptability. The KBP@KH hydrogel facilitated angiogenesis and suppressed the production of inflammatory factors. Overall, the KBP@KH hydrogel dressing was characterized by its user-friendly nature, safety, and high efficiency.
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Bioactive Materials
·
2024
·
IF 18
Xuan Bai,Wenan Peng,Ying Tang,Ziming Wang,Jingmei Guo,Fangfang Song,Hongye Yang,Cui Huang
Periodontitis is an inflammatory disease caused by bacterial biofilms, which leads to the destruction of periodontal tissue. Current treatments, such as mechanical cleaning and antibiotics, struggle to effectively address the persistent biofilms, inflammation, and tissue damage. A new approach involves developing a Janus nanomotor (J-CeM@Au) by coating cerium dioxide-doped mesoporous silica (CeM) with gold nanoparticles (AuNPs). This nanomotor exhibits thermophoretic motion when exposed to near-infrared (NIR) laser light due to the temperature gradient produced by the photothermal effects of asymmetrically distributed AuNPs. The NIR laser provides the energy for propulsion and activates the nanomotor's antibacterial properties, allowing it to penetrate biofilms and kill bacteria. Additionally, the nanomotor's ability to scavenge reactive oxygen species (ROS) can modulate the immune response and create a regenerative environment, promoting the healing of periodontal tissue. Overall, this multifunctional nanomotor offers a promising new approach for treating periodontitis by simultaneously addressing biofilm management and immune modulation with autonomous movement.
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CHEMICAL ENGINEERING JOURNAL
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2024
·
IF 13.3
Panxianzhi Ni,Dengbinpei Duan,Shuting Xiong,Meng Zhong,Can Huang,Jing Shan,Tun Yuan,Jie Liang,Yujiang Fan,Xingdong Zhang
Gastric ulcer (GU) is currently one of the most serious and common gastrointestinal diseases worldwide, severely affects the quality of life of patients. However, treatment strategies have limitations, such as drug safety and lack of repair specificity. In this work, we developed a polyethyleneimine/polyacrylic acid/lactose-modified chitosan (PPCL) hydrogel to repair gastric ulcers. This hydrogel was characterized by robust tissue adhesion, low swelling rate, gastric acid fluid resistance, potent antioxidants and good biocompatibility, which could act as a physical barrier to prevent gastric acid and digestive enzymes from further destroying ulcers. In vivo data from a rat GU model confirmed that this hydrogel effectively promoted gastric ulcer healing, and the therapeutic effect was better than that of commercial gastric mucosal protectants. Further mechanistic research identified that the hydrogel accelerated GU healing by alleviating oxidative stress, promoting reepithelization, angiogenesis and mucosal repair. Our findings revealed that the PPCL hydrogel provides a promising therapeutic approach for healing gastric ulcer.
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Acta Biomaterialia
·
2024
·
IF 9.4
Zhicheng Tong,Yuanzhu Ma,Qiushi Liang,Tao Lei,Hongwei Wu,Xianzhu Zhang,Yishan Chen,Xihao Pan,Xiaozhao Wang,Huimin Li,Junxin Lin,Wei Wei,Chong Teng
Superficial cartilage defects represent the most prevalent type of cartilage injury encountered in clinical settings, posing significant treatment challenges. Here, we fabricated a cartilage extracellular matrix mimic hydrogel (GHC, consisting of Gelatin, Hyaluronic acid, and Chondroitin sulfate) to avoid the exacerbation of cartilage deterioration, which is often driven by the accumulation of reactive oxygen species (ROS) and a pro-inflammatory microenvironment. The GHC hydrogel exhibited multifunctional properties, including in situ formation, tissue adhesiveness, anti-ROS capabilities, and the promotion of chondrogenesis. The enhancement of tissue adhesion was achieved by chemically modifying hyaluronic acid and chondroitin sulfate with o-nitrobenzene, enabling a covalent connection to the cartilage surface upon light irradiation. In vitro characterization revealed that GHC hydrogel facilitated chondrocyte adhesion, migration, and differentiation into cartilage. Additionally, GHC hydrogels demonstrated the ability to scavenge ROS in vitro and inhibit the production of inflammatory factors by chondrocytes. In the animal model of superficial cartilage injury, the hydrogel effectively promoted cartilage ECM regeneration and facilitated the interface integration between the host tissue and the material. These findings suggest that the multifunctional GHC hydrogels hold considerable promise as a strategy for cartilage defect repair. Statement of Significance : Superficial cartilage defects represent the most prevalent type of cartilage injury encountered in the clinic. Previous cartilage tissue engineering materials are only suitable for full-thickness cartilage defects or osteochondral defects. Here, we developed a multifunctional GHC hydrogel composed of gelatin, hyaluronic acid, and chondroitin sulfate, which are natural cartilage extracellular matrix components. The drug-free and cell-free hydrogel not only avoids immune rejection and drug toxicity, but also shows good mechanical properties and biocompatibility. More importantly, the GHC hydrogel could adhere tightly to the superficial cartilage defects and promote cartilage regeneration while protecting against oxidation. This natural ingredients and multifunctional hydrogel is a potential material for repairing superficial cartilage defects.
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高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2024
·
IF 13.3
Wenjing Wang,Guangrong Lu,Zhichao Deng,Huanyu Li,Wenfang He,Shouxing Yang,Yuanyuan Zhu,Chenxi Xu,Yujie Zhang,Lanqi Wang,Xiaoling Huang,Mingzhen Zhang,Changlong Xu
Ulcerative colitis (UC), a prevalent form of inflammatory bowel disease (IBD), is characterized by the presence of chronic, nonspecific, and recurring inflammation in the intestine. Current therapies are insufficient in addressing the effective modulation of the intestinal oxidative stress-inflammation cycle, the repair of the intestinal mechanical barrier, and the regulation of gut microbiota and metabolites. There is a need for a comprehensive approach to orchestrate intestinal homeostasis more effectively. For this purpose, biocompatible antioxidant carbon dots nanozymes (GH-CDs) were synthesized based on glucose and D-histidine using a microwave-assisted method for the systematic management of intestinal inflammation. It was demonstrated that GH-CDs possessed excellent reactive oxygen/nitrogen species (ROS/RNS) scavenging capacities, thus modulating oxidative stress-induced damage and mitigating inflammation by inhibiting the TNF, MAPK, PI3K-Akt, NF-κB, and JAK-STAT signaling pathways. For in vivo experiments, GH-CDs have demonstrated both protective and therapeutic effects in mitigating colitis by reducing ROS levels, decreasing the infiltration of M1-type macrophages, suppressing the release of pro-inflammatory cytokines, and repairing intestinal mechanical and chemical barriers. Importantly, GH-CDs also influenced the gut microbiome to achieve a more beneficial state, which was accomplished by enhancing bacterial diversity and altering the microbial composition towards an anti-inflammatory type. Additionally, GH-CDs supported the biosynthesis of secondary bile acids and isoflavonoids. In conclusion, with excellent biocompatibility, GH-CDs will be a promising strategy for UC by comprehensively orchestrating intestinal homeostasis.
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Particle and Fibre Toxicology
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2016
·Vol. 13
·期 1
·1-13
·
IF 8.649
Guo Hua,Zhang Jing,Boudreau Mary,Meng Jie,Yin Jun-jie,Liu Jian,Xu Haiyan
Background Administration of silver nanoparticles (AgNPs) to mice could result in their distribution and accumulation in multiple organs, with notable prominence in liver, lungs, and kidneys. However, how AgNPs transport through blood vesicular system to reach the target organs is unclear, and the precise differences in the mechanisms of toxicity between AgNPs and silver ions still remain elusive. In the present research, the pathological changes on these target organs with a focus on inter-endothelial junction was investigated to gain a new insight of AgNPs toxicity by comparing the mechanisms of action of AgNPs and AgNO3.Methods We investigated the in vitro cytotoxicity of either citrated-coated AgNPs (10, 75, and 110 nm) or silver nitrate (AgNO3) following 24 h incubations (1–40 μg/mL) in the presence of primary human umbilical vein endothelial cells (HUVEC). Meanwhile, we detected the effects of AgNPs on intercellular conjunction and intracellular ROS by VE-cadherin staining and 2′, 7′-dichlorodihydrofluorescein diacetate (DCFH-DA) assay, respectively. To assess in vivo toxicity, we administered single or multiple intravenous injections (25 μg Ag for AgNPs and 2.5 μg Ag for AgNO3 per dose) to mice.Results In the in vitro study, the TEM observation showed that AgNPs were taken up by endothelial cells while AgNO3 was taken up little. Meanwhile AgNPs incubation induced the elevation of intracellular ROS and down-regulation of VE-cadherin between the endothelial cells and affected the cytoskeleton actin reorganization, which could be rescued by antioxidant N-acetylcysteine. In contrast, AgNO3 caused direct cell death when the concentration was higher than 20 μg/mL and without ROS induction at lower concentration. The release of AgNPs from leaking vessels induced peripheral inflammation in the liver, lungs, and kidneys, and the severity increased in proportion to the diameter of the AgNPs used.Conclusion It is AgNPs but not AgNO3 that were taken up by vascular endothelial cells and induced intracellular ROS elevated, which was closely related to disruption of the integrity of endothelial layer. The AgNPs-induced leakiness of endothelial cells could mediate the common peripheral inflammation in liver, kidney and lung through intravenous exposure.
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BIOMEDICINE & PHARMACOTHERAPY
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2017
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IF 2.759
Yanyan Zhu,Yameng Jiang,Lei Shi,Linying Du,Xiaodong Xu,Enxia Wang,Yong Sun,Xin Guo,Boyang Zou,Huaxin Wang,Changyuan Wang,Lidan Sun,Yuhong Zhen
7- O -Geranylquercetin (GQ) is a novel O -alkylated derivate of quercetin . In this study, we evaluated its apoptosis induction effects in human gastric cancer cell lines SGC-7901 and MGC-803 and explored the potential molecular mechanisms. The results demonstrated that GQ lowered viability of SGC-7901 and MGC-803 cells in a dose- and time-dependent manner without apparent cytotoxicity to human gastric epithelial cell line GES-1. GQ could induce apoptosis in SGC-7901 and MGC-803cells, and arrest the gastric cancer cells at G2/M phase. Mechanism study showed that GQ triggered generation of reactive oxygen species (ROS), then activated p38 and JNK signaling pathways , subsequently led to mitochondrial impairment by regulating the expression of Bcl-2, Bcl-xl and Bax, and finally promoted the release of cytochrome c and the activation of caspases to induce apoptosis. In addition, Z-VAD-FMK (caspase inhibitor) could reverse GQ-induced apoptosis. SB203580 (p38 inhibitor) and SP600125 (JNK inhibitor) could rescue GQ-induced cell death and attenuate mitochondrial signal pathway activation. Furthermore, NAC (ROS inhibitor) could rescue GQ-induced cell death, reduce ROS generation, decrease the phosphorylation of p38 and JNK, and then attenuate the activation of mitochondrial signal pathway. Taken together, GQ induces caspase-dependent apoptosis in gastric cancer cells through activating ROS-MAPK mediated mitochondrial signal pathway. This study highlights the potential use of GQ as a gastric cancer therapeutic agent.
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CELLULAR AND MOLECULAR NEUROBIOLOGY
·
2016
·Vol. 36
·期 8
·1365-1375
·
IF 2.328
Lin Xuemei,Wu Songdi,Wang Qing,Shi Yaling,Liu Guozheng,Zhi Jin,Wang Fang
Neuronal oxidative stress (OS) injury has been proven to be associated with many neurodegenerative diseases, and thus, antioxidation treatment is an effective method for treating these diseases. Saikosaponin-D (SSD) is a sapogenin extracted from Bupleurum falcatum and has been shown to have many pharmacological activities. The main purpose of this study was to investigate whether and how SSD protects PC12 cells from H 2 O 2 -induced apoptosis. The non-toxic level of SSD significantly mitigated the H 2 O 2 -induced decrease in cell viability, reduced the apoptosis rate, improved the nuclear morphology, and reduced caspase-3 activation and poly ADP-ribose polymerase (PARP) cleavage. Additionally, exogenous H 2 O 2 -induced apoptosis by damaging the intracellular antioxidation system. SSD significantly slowed the H 2 O 2 -induced release of malonic dialdehyde (MDA) and lactate dehydrogenase and increased the activity of superoxide dismutase (SOD) and the total antioxidant capacity, thereby reducing apoptosis. More importantly, SSD effectively blocked H 2 O 2 -induced phosphorylation of extracellular-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38MAPK), and specific inhibitors of ERK, JNK, and p38-reduced OS injury and apoptosis, suggesting that SSD reduces OS injury and apoptosis via MAPK signalling pathways. Finally, we confirmed that SSD significantly reduced H 2 O 2 -induced reactive oxygen species (ROS) accumulation, and the ROS inhibitor blocked the apoptosis caused by MAPK activation and cellular oxidative damage. In short, our study confirmed that SSD reduces H 2 O 2 -induced PC12 cell apoptosis by removing ROS and blocking MAPK-dependent oxidative damage.
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BIOMATERIALS
·
2017
·
IF 8.402
Haibin Wu,Fangyuan Li,Shuaifei Wang,Jingxiong Lu,Jinquan Li,Yang Du,Xiaolian Sun,Xiaoyuan Chen,Jianqing Gao,Daishun Ling
Restoration of tissue integrity and tissue function of wounded skin are both essential for wound repair and regeneration, while synergistic promotion of the two remains elusive. Since elevated reactive oxygen species (ROS) production in the injured site has been implicated in triggering a set of deleterious effects such as cellular senescence, fibrotic scarring, and inflammation, it is speculated that alleviating oxidative stress in the microenvironment of injured site would be beneficial to promote regenerative wound healing. In this study, a highly versatile ROS-scavenging tissue adhesive nanocomposite is synthesized by immobilizing ultrasmall ceria nanocrystals onto the surface of uniform mesoporous silica nanoparticles (MSN). The ceria nanocrystals decorated MSN (MSN-Ceria) not only has strong tissue adhesion strength , but also significantly restricts ROS exacerbation mediated deleterious effects, which efficiently accelerates the wound healing process, and more importantly, the wound area exhibits an unexpected regenerative healing characteristic featured by marked skin appendage morphogenesis and limited scar formation. This strategy can also be adapted to other wound repair where both ROS-scavenging activity and tissue adhesive ability matter.
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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
·
2024
·Vol. 28
·期 20
·e70127
·
IF 4.3
Ming Zhang,Guan-Chun Dai,Yuan-Wei Zhang,Pan-Pan Lu,Hao Wang,Ying-Juan Li,Yun-Feng Rui
Diabetic calcific tendinopathy is the leading cause of chronic pain, mobility restriction, and tendon rupture in patients with diabetes. Tendon stem/progenitor cells (TSPCs) have been implicated in the development of diabetic calcified tendinopathy, but the molecular mechanisms remain unclear. This study found that diabetic tendons have a hyperoxic environment, characterized by increased oxygen delivery channels and carriers. In hyperoxic environment, TSPCs showed enhanced osteogenic differentiation and increased levels of reactive oxygen species (ROS). Additionally, hypoxia-inducible factor-1a (HIF-1a), a protein involved in regulating cellular responses to hyperoxia, was decreased in TSPCs by the ubiquitin-proteasome system. By intervening with antioxidant N-acetyl-L-cysteine (NAC) and overexpressing HIF-1a, we discovered that blocking the ROS/HIF-1a signalling axis significantly inhibited the osteogenic differentiation ability of TSPCs. Animal experiments further confirmed that hyperoxic environment could cause calcification in the Achilles tendon tissue of rats, while NAC intervention prevented calcification. These findings demonstrate that hyperoxia in diabetic tendons promotes osteogenic differentiation of TSPCs through the ROS/HIF-1a signalling axis. This study provides a new theoretical basis and research target for preventing and treating diabetic calcified tendinopathy.
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MATERIALS & DESIGN
·
2024
·
IF 7.6
Huidong Wang,Jiadong Guo,Yangzi Yang,Ning Wang,Xiao Yang,Liang Deng,Xiankun Cao,Zhaoyang Ran,Dong Fang,Kang Xu,Yingchun Zhu,Jie Zhao,Jingke Fu,Yongqiang Hao
With the clinical prevalence of drug-resistant pathogenic bacteria, developing non-antibiotic strategies to treat multi-drug-resistant bacterial infections is urgent yet challenging. Ferroptosis is a non-apoptotic form of regulated cell death that can overcome drug resistance. Emerging evidence shows the potential of triggering ferroptosis-like for anti-infection therapy, but the direct delivery of iron species is inefficient and may cause detrimental effects. Herein, CuFeS 2 nanozyme is revealed as a ferroptosis-like initiator to eradicate bacterial infections for effective anti-infection therapy. Upon activating by visible light irradiation or hydrogen peroxide, the as-prepared CuFeS 2 nanozyme can significantly expedite reactive oxygen species generation, deplete intracellular glutathione, and interfere with respiratory metabolisms, resulting in lipid peroxidation-driven ferroptotic damage. Additionally, the CuFeS 2 displays good photothermal conversion capacity under near-infrared light irradiation, further augmenting the antibacterial efficiency. Accordingly, the CuFeS 2 nanozyme shows potent antibacterial activity against Gram-negative Escherichia coli and Gram-positive methicillin-resistant Staphylococcus aureus strains in vitro . Moreover, it shows excellent biocompatibility and robust anti-infection effects in MRSA-infected wounds in vivo . This ferroptosis-like antibacterial strategy may open up new insights into the treatment of drug-resistant pathogen infection.
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Nanoscale
·
2024
·
IF 5.8
Bihui Zhu,Zhenyang Zhao,Sujiao Cao,Yimin Sun,Liyun Wang,Songya Huang,Chong Cheng,Lang Ma,Li Qiu
The creation of atomic catalytic centers has emerged as a conducive path to design efficient nanobiocatalysts to serve as artificial antioxidases (AAOs) that can mimic the function of natural antioxidases to scavenge noxious reactive oxygen species (ROS) for protecting stem cells and promoting tissue regeneration. However, the fundamental mechanisms of diverse single-atom sites for ROS biocatalysis remain ambiguous. Herein, we show that highly spontaneous spin polarization mediates the hitherto unclear origin of H2O2-elimination activities in engineering ferromagnetic element (Fe, Co, Ni)-based AAOs with atomic centers. The experimental and theoretical results reveal that Fe-AAO exhibits the best catalase-like kinetics and turnover number, while Co-AAO shows the highest glutathione peroxidase-like activity and turnover number. Furthermore, our investigations prove that both Fe-AAO and Co-AAO can effectively secure the functions of stem cells in high ROS microenvironments and promote the repair of injured tendon tissue by scavenging H2O2 and other ROS. We believe that the proposed highly spontaneous spin polarization engineering of ferromagnetic element-based AAOs will provide essential guidance and practical opportunities for developing efficient AAOs for eliminating ROS, protecting stem cells, and accelerating tissue regeneration.
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