Biomedical Optics Express
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2021
·Vol. 12
·期 11
·6984-6994
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IF 3.732
Xinyan Jiang,Xinyan Jiang,Rui Pu,Rui Pu,Cheng Wang,Jiale Xu,Yaohui Tang,Shuhong Qi,Shuhong Qi,Qiuqiang Zhan,Xunbin Wei,Xunbin Wei,Xunbin Wei,Bobo Gu
Acquired brain injury (ABI), which is the umbrella term for all brain injuries, is one of the most dangerous diseases resulting in high morbidity and mortality, making it extremely significant to early diagnosis of ABI. Current methods, which are mainly composed of X-ray computed tomography and magnetic resonance angiography, remain limited in diagnosis of ABI with respect to limited spatial resolution and long scanning times. Here, we reported through-skull fluorescence imaging of mouse cerebral vasculature without craniotomy, utilizing the fluorescence of down-conversion nanoparticles (DCNPs) in the 1.3 - 1.7 μm near-infrared window (NIR-II window). Due to its high spatial resolution of 22.79 μm, the NIR-II fluorescence imaging method could quickly distinguish the brain injury region of mice after performing the stab wound injury (traumatic brain injury) and ischemic stroke (non-traumatic brain injury), enabling it a powerful tool in the noninvasive and early diagnosis of ABI.
研究领域:
医学影像学
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神经科学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
ANNALS OF BIOMEDICAL ENGINEERING
·
2022
·Vol. 50
·期 9
·1038-1052
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IF 4.219
Du Zhibo,Li Zhijie,Wang Peng,Wang Xinghao,Zhang Jiarui,Zhuang Zhuo,Liu Zhanli
Intracranial pressure (ICP) during the interaction between blast wave and the head is a crucial evaluation criterion for blast-induced traumatic brain injury (bTBI). ICP variation is mainly induced by the blast wave transmission and skull deformation. However, how the skull deformation influences the ICP remains unclear, which is meaningful for mitigating bTBI. In this study, both experimental and numerical models are developed to elucidate the effect of skull deformation on ICP variation. Firstly, we performed the shock tube experiment of the high-fidelity surrogate head to measure the ICP, the blast overpressure, and the skull surface strain of specific positions. The results show that the ICP profiles of all measured points show oscillations with positive and negative change, and the variation is consistent with the skull surface strain. Further numerical analysis reveals that when the blast wave reaches the measured point, the peak overpressure transmits directly through the skull to the brain, forming the local positive ICP peak, and the impulse induces the local inward deformation of the skull. As the peak overpressure passes through, the blast impulse impacts the nearby skull supported by the soft and incompressible brain tissue and extrudes the skull outward in the initial position. The inward and outward skull deformation leads to the oscillation of ICP. These numerical analyses agree with experimental results, which explain the appearance of negative and positive ICP peaks and the synchronization of negative ICP with surface strain. The study has implications for medical injury diagnosis and protective equipment design.
研究领域:
生物力学
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医学工程
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创伤医学
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DOI
高影响因子
Science Advances
·
2024
·Vol. 10
·期 2
·
IF 11.7
Xuefeng Zhang,Xuyang Huang,Diancheng Hang,Jiaqi Jin,Shanshan Li,Yufu Zhu,Hongmei Liu
Posttraumatic neuroinflammation is a key driver of secondary injury after traumatic brain injury (TBI). Pyroptosis, a proinflammatory form of programmed cell death, considerably activates strong neuroinflammation and amplifies the inflammatory response by releasing inflammatory contents. Therefore, treatments targeting pyroptosis may have beneficial effects on the treatment of secondary brain damage after TBI. Here, a cysteine-alanine-glutamine-lysine peptide–modified β-lactoglobulin (β-LG) nanoparticle was constructed to deliver disulfiram (DSF), C-β-LG/DSF, to inhibit pyroptosis and decrease neuroinflammation, thereby preventing TBI-induced secondary injury. In the post-TBI mice model, C-β-LG/DSF selectively targets the injured brain, increases DSF accumulation, and extends the time of the systemic circulation of DSF. C-β-LG/DSF can alleviate brain edema and inflammatory response, inhibit secondary brain injury, promote learning, and improve memory recovery in mice after trauma. Therefore, this study likely provided a potential approach for reducing the secondary spread of TBI.
研究领域:
神经科学
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药理学
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纳米技术
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炎症生物学
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产品关联
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Bowen Jia,Yuchen Yao,Yejia Xu,Yang Zhao,Jing Li,Yumeng Wu,Xiaofeng Zeng,Shijun Hong,Qianqian Li,Xuexia Liu,Chengliang Luo
Traumatic brain injury (TBI) is a major global health issue, causing blood–brain barrier disruption, neuroinflammation, and neuronal damage. Current therapies are limited and failed to address key pathological mechanisms like ferroptosis, oxidative stress, and inflammation, highlighting the need for novel treatments. Recent advances in nanomedicine, particularly nanozymes, offer promising solutions. Copper-based ultrasmall nanozymes, with excellent catalytic activity and biocompatibility, have shown potential in mitigating ferroptosis and oxidative stress. In this study, we developed polyethylene glycol-modified Cu 5.4 O (Cu 5.4 O-PEG), a nanomaterial with superior blood–brain barrier penetration and biocompatibility. Cu 5.4 O-PEG demonstrated no cytotoxicity and significantly reduced oxidative stress and ferroptosis in both in vitro and in vivo models, improving motor and cognitive functions in murine TBI models. The therapeutic effects were mediated through multiple mechanisms, including inhibition of the Fenton reaction, scavenging of reactive oxygen species (ROS), and reducing iron deposition, effectively limiting tissue damage. Proteomic analysis revealed modulation of ferroptosis-related proteins and activation of protective pathways related to transferrin receptor 1 (TfR1). Furthermore, using AAV-mediated knockdown of TfR1 in mice, we observed significant reductions in lipid peroxidation markers such as ACSL4, COX2, and 4HNE, indicating a decrease in iron-induced damage. Histological analysis showed reduced iron deposition, and improved neuronal morphology in TfR1 knockdown mice underwent TBI, indicating knockdown of TfR1 could alleviate TBI-indued ferroptosis and iron-dependent neurodegeneration. Taken together, these data imply that Cu 5.4 O-PEG presents a neuroprotective strategy for improving cerebral recovery after TBI, at least partly by inhibiting TfR1-mediated ferroptosis.
研究领域:
神经科学
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纳米医学
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药理学
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产品关联
DOI
高影响因子
ACS Nano
·
2024
·
IF 15.8
Mingxia Jiao,Xiaoqi Li,Hui Liu,Peng Cai,Xiling Yang,Kevin J. McHugh,Bowen Zheng,Jiachen Sun,Peisen Zhang,Xiliang Luo,Lihong Jing
Surgical intervention is the most common first-line treatment for severe traumatic brain injuries (TBIs) associated with high intracranial pressure, while the complexity of these surgical procedures often results in complications. Surgeons often struggle to comprehensively evaluate the TBI status, making it difficult to select the optimal intervention strategy. Here, we introduce a fluorescence imaging-based technology that uses high-quality silver indium selenide-based quantum dots (QDs) for integrated TBI diagnosis and surgical guidance. These engineered, poly(ethylene glycol)-capped QDs emit in the near-infrared region, are resistant to phagocytosis, and importantly, are ultrastable after the epitaxial growth of an aluminum-doped zinc sulfide shell in the aqueous phase that renders the QDs resistant to long-term light irradiation and complex physiological environments. We found that intravenous injection of QDs enabled both the precise diagnosis of TBI in a mouse model and, more importantly, the comprehensive evaluation of the TBI status before, during, and after an operation to distinguish intracranial from superficial hemorrhages, provide real-time monitoring of the secondary hemorrhage, and guide the decision making on the evacuation of intracranial hematomas. This QD-based diagnostic and monitoring system could ultimately complement existing clinical tools for treating TBI, which may help surgeons improve patient outcomes and avoid unnecessary procedures.
研究领域:
生物医学工程
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神经外科
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材料科学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Chemistry
·
2021
·
IF 5.221
Cai Wei,Wu Qi,Yan Zhi Zhong,He Wei-Zhen,Zhou Xiao-Ming,Zhou Long-Jiang,Zhang Jian-Yong,Zhang Xin
Subarachnoid hemorrhage (SAH) is a fatal disease. Within 72 h of SAH, the intracranial blood-brain barrier (BBB) is destroyed, and the nerve cells have responses such as autophagy, apoptosis, and oxidative stress. Antioxidation is an essential treatment of SAH. Astaxanthin (ATX) induces cells’ antioxidant behaviors by regulating related signal pathways to reduce the damage of brain oxidative stress, inflammation, and apoptosis. Because of its easy degradability and low bioavailability, ATX is mainly encapsulated with stimulus-responsive nanocarriers to improve its stability, making it rapidly release in the brain and efficiently enter the lesion tissue. In this study, the ultrasonic cavitation agent perfluorocarbon (PFH), ATX, and fluorescent dye IR780 were loaded with polydopamine (PDA) to prepare a US triggered release nanoparticles (AUT NPs). The core-shell structure of AUT NPs formed a physical barrier to improve the bioavailability of ATX. AUT NPs have high ATX loading capacity and US responsiveness. The experimental results show that the AUT NPs have high stability in the physiological environment. Both US and pH stimuli can trigger the release. Under US, PFH breaks through the rigid shell. The structure of AUT NPs is destroyed in situ, releasing the loaded drugs into neuronal cells to realize the antioxidant and antiapoptotic effects. The in vivo experiment results show that the AUT NPs have good biosafety. They release the drugs in the brain under stimuli. The in vivo treatment results also show that AUT NPs have an excellent therapeutic effect. This approach presents an experimental basis for the establishment of Innovative SAH treatments.
研究领域:
神经科学
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药学
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产品关联
DOI
PubMed
高影响因子
LIFE SCIENCES
·
2025
·
IF 5.1
Kaiji Li,Jinchao Wang,Yalong Gao,Xin Chen,Ruilong Peng,Lei Li,Cong Wang,Tuo Li,Shu Zhang,Guili Yang,Jianning Zhang
Aims Traumatic brain injury-induced coagulopathy (TBI-IC) frequently occurs after TBI, exacerbating the severity of TBI and affecting patient prognosis. Benzbromarone (BBR) is commonly used to treat hyperuricemia; however, its protective effects against TBI-IC remain unknown. Therefore, we explored whether BBR could improve TBI. Materials and methods C57BL/6 wild-type mice were subjected to fluid percussion injury to mimic TBI, and BBR was administered intraperitoneally 30 min after TBI. Magnetic resonance imaging (MRI) and Evans blue dye extravasation were used to assess the prognosis, tail bleeding time, ELISA, and coagulation tests assess coagulation function. We further explored the potential mechanism by which BBR alleviates hypercoagulation after TBI using flow cytometry. Key findings The intraperitoneally injected BBR group showed improved survival and neurological severity scores compared to the TBI group. Subsequently, we found that hypercoagulability developed 3 h after TBI and that the administration of BBR improved this hypercoagulability. BBR also reduced the degree of platelet phosphatidylserine (PS) exposure after TBI, platelet activation, and Ca2+ overload, in addition to inhibition of scramblase activity in procoagulant platelets. Significance Our findings indicate that BBR reduces PS externalization by inhibiting TMEM16F expression, thereby improving blood hypercoagulability after TBI.
研究领域:
神经科学
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药理学
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血液学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
COMPOSITES PART B-ENGINEERING
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2022
·
IF 11.322
Ye Li,Min Wang,Meng Sun,Xinxin Wang,Dandan Pei,Bo Lei,Ang Li
Traumatic brain injury (TBI) leads to high rates of morbidity and mortality worldwide with few effective treatments. Excessive oxidative stress and local inflammation at the injury site are considered as the critical factors that determine the therapeutic outcome. In our previous study, stem cells from human exfoliated deciduous teeth-derived exosomes (SHED-Exo) promoted functional recovery of TBI by amelioration of neuro-inflammation. However, the effect was restricted due to unsustainable exosome release and existed oxidative stress that aggravate secondary insult of TBI. To obtain a long-time anti-inflammatory effect of SHED-Exo and attenuate oxidative stress simultaneously, we designed a bioactive antioxidant poly (citrate-gallic acid)-based hybrid hydrogel (FPGEGa) that encapsulate SHED-Exo for treating TBI. The thermosensitive, injectable, self-healing and antioxidant FPGEGa presented ultralong sustained release of SHED-Exo (above 21 days) and significantly decreased the intracellular ROS production of microglia in the central nervous system. FPGEGa carrying SHED-Exo (FPGEGa@SHED-Exo) exhibited better anti-inflammatory potential on microglia, by promoting M2 (anti-inflammatory) polarization and inhibiting M1 (pro-inflammatory) polarization. FPGEGa@SHED-Exo could improve the neuro-regeneration of TBI rats by rescuing damaged motor functions in rats as well as regenerating impaired cortical tissues. The present work suggested that SHED-Exo engineered bioactive antioxidative hydrogel may be promising in achieving satisfactory functional recovery in TBI and other related neurological disorders.
研究领域:
生物材料学
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神经科学
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再生医学
✓ 已验证
DOI
高影响因子
Materials Today Communications
·
2021
·
IF 3.383
Qifeng Li,Yalong Gao,Jun Shen,Xiaoyu Mu,Junying Wang,Lufei Ouyang,Ke Chen,Hua He,Jiahui Pei,Qinjuan Ren,Si Sun,Haile Liu,Lei Zhou,Yuanming Sun,Wei Long,Jianning Zhang,Xiao-Dong Zhang
Hypoxemia as one of the most common symptoms of traumatic brain injury (TBI) can significantly exacerbate the development of secondary damage, which further contributes to generating large numbers of neurotoxic factors such as reactive oxygen and nitrogen species (RONS), pro-inflammatory cytokine and chemokine. Here, we developed a kind of quantum dots as catalase-mimic and multiple free radical scavengers by means of the microwave heating polymerization of l -lysine. Hydrogen peroxide as overproduced radicals can be decomposed to supply oxygen, contributing to improving the hypoxic condition in brain. Simultaneously, other traditional RONS such as O 2 − , OH, NO and ONOO − can be eliminated by the quantum dots. The total ROS level is back to normal after the quantum dots treatment, promoting the H 2 O 2 /LPS-stimulated cell survival in vitro . Oxidative stress induced by hypoxic brain injury is restored by the quantum dots intravenous injection, leading to the protection of neural cells in vivo . Additionally, the quantum dots can improve the spatial learning and memory of TBI mice by water maze test. This work provides a new perspective for the therapy of hypoxic brain injury.
研究领域:
神经科学
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药学
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材料科学
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生物医学工程
✓ 已验证
产品关联
DOI
高影响因子
TOXICOLOGY MECHANISMS AND METHODS
·
2025
·
IF 2.7
Dan Wang,Hui Sun,Kerong Hai,Ningkang Li,Yang Gu,Zengrui Ma
Traumatic brain injury (TBI), a prevalent neurological disorder in clinical practice, is primarily induced by external trauma. Propofol has been reported to alleviate the symptoms associated with TBI. In this study, a TBI model was established in mice using the controlled cortical impact (CCI) method. After treatment with propofol and BML-275, neuronal damage in the TBI model was assessed through the modified Neurological Severity Score (mNSS), Hematoxylin and Eosin (HE) staining, and Nissl staining. To investigate the role of the AMPK/SIRT1 pathway in propofol-regulated TBI, AMPKα-silenced vectors and overexpressed SIRT1 vectors were transfected. Western blot was performed to evaluate the expression of proteins involved in the AMPK/SIRT1 pathway and pyroptosis markers. The regulatory impact of Th17/Treg balance was examined by detecting the key transcription factors RORγt and FOXP3 through immunofluorescent staining and RT-qPCR. Enzyme-linked immunosorbent assay (ELISA) was used to measure IL-17 and IL-10 concentrations. Results showed that propofol significantly reduced neuronal injury in the TBI model, an effect that was reversed by BML-275. Moreover, propofol mitigated pyroptosis by downregulating Caspase-1 and GSDMD-N expression post-TBI. Propofol inhibited Th17 differentiation while promoting Treg differentiation by modulating RORγt/FOXP3 and IL-17/IL-10 levels. Silencing AMPKα markedly diminished propofol’s effects on Th17 and Treg differentiation, with these effects being reversed upon SIRT1 overexpression. Propofol suppressed neuronal pyroptosis through the regulation of Th17/Treg balance via activation of the AMPK/SIRT1 pathway. These findings suggest propofol exerts a protective effect against neuronal damage following TBI, potentially through the modulation of the Th17/Treg balance and AMPK/SIRT1 signaling pathway.
研究领域:
神经科学
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免疫学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACS Applied Materials & Interfaces
·
2025
·
IF 8.2
Jing Xu,Danyi Shen,Yao Wang,Xingyue Han,Xinning Dong,Xin Chen,Haifeng Shu,Jianwen Hou,Sixun Yu
Traumatic brain injury (TBI) can trigger a series of complex physiological responses, with iron overload and neuronal ferroptosis playing particularly pivotal roles. These processes exacerbate secondary brain injury and significantly deteriorate neurological function. To address this challenge, this study developed an innovative local drug delivery strategy: an injectable, post-traumatic microenvironment-responsive hydrogel. The hydrogel, composed of tannic acid (TA) and quaternized chitosan (QCS), is designed to alleviate neurological deficits secondary brain injury following TBI through its anti-ferroptosis mechanism. In vitro, a ferroptosis model was established using HT22 cells treated with the ferroptosis inducer RSL-3, demonstrating the hydrogel’s antioxidant capacity in the TBI-like conditions. The results showed that the hydrogel significantly restored cell viability, reversed iron accumulation, alleviated lipid peroxidation, and restored mitochondrial function. Further in vivo experiments in the TBI model showed that the TA/QCS hydrogel not only effectively inhibited neuronal degeneration, reduced iron accumulation, and lipid peroxidation but also restored mitochondrial function in neurons. Additionally, the hydrogel significantly attenuated neuroinflammation by inhibiting the activation of microglia and astrocytes, thereby facilitating neurological recovery after TBI. This study offers novel insights into TBI management strategies aimed at preventing the progression of a secondary injury.
研究领域:
神经科学
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药学
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生物材料学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CNS Neuroscience & Therapeutics
·
2025
·Vol. 31
·期 7
·e70502
·
IF 5
Xin Shu,Xinxin Zou,Jingxuan Zhang,Xu Fang,Xinyu Wang,Hui Wu,Xuan He,Dujuan Sha
Background Neuroinflammation is an important factor in ischemic stroke. Dehydrocostus lactone (DHC) plays an anti-inflammatory role in certain diseases. However, the role of DHC in neuroinflammation after ischemic stroke remains unclear. Methods DHC was administered to lipopolysaccharide (LPS)-treated BV2 cells and a middle cerebral artery occlusion (MCAO) model to detect the levels of inflammatory factors using quantitative real-time PCR, western blotting, and behavioral tests. Morphological changes in microglia were observed using immunofluorescence. The Swiss Target Prediction database was used to predict the target of DHC. Finally, a specific inhibitor of the target protein was used to investigate its potential synergistic role in neuroinflammation, both with and without being combined with DHC. Results The expression of inflammation-related factors both in vivo and in vitro was improved by DHC, and the neurological deficits in mice after MCAO were improved in the DHC administration group. In addition, the Swiss Target Prediction showed that CYP2A6 was a target of DHC. Specifically, the combination of DHC with the CYP2A6 inhibitor showed that DHC exerts anti-inflammatory effects in a CYP2A6-dependent manner. Conclusion Mechanistically, DHC inhibited neuroinflammation by binding to the target CYP2A6. Our study suggests that DHC is a promising new strategy for treating ischemic stroke.
研究领域:
神经生物学
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药理学
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免疫学
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生物化学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）