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Neutrophil extracellular traps mediate neuro-immunothrombosis

Neural regeneration Research 2024年第8期19卷 1734-1740页

作者： Jianbo Lou Jianning Zhang Quanjun Deng Xin Chen Department of neurosurgery Tianjin Medical University General HospitalTianjinChina Tianjin neurological Institute Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous SystemMinistry of EducationTianjin Key Laboratory of InjuriesVariations and Regeneration of Nervous SystemTianjinChina

Neutrophil extracellular traps are primarily composed of DNA and histones and are released by neutrophils to promote inflammation and thrombosis when stimulated by various inflammato ry *** extracellular trap formation occurs through lytic and non-lytic pathways that can be further classified by formation ***,von Willebrand factor,fibrin,and many other factors participate in the interplay between inflammation and *** summarizes the intricate interplay between inflammation and thrombosis during neural development and the pathogenesis of neurological diseases,providing cutting-edge insights into post-neurotrauma thrombotic *** blood-brain barrier defends the brain and spinal cord against external assaults,and neutrophil extracellular trap involvement in blood-brain barrier disruption and immunothrombosis contributes substantially to secondary injuries in neurological *** research is needed to understand how neutrophil extracellular traps promote blood-brain barrier disruption and immunothrombosis,but recent studies have demonstrated that neutrophil extracellular traps play a crucial role in immunothrombosis,and identified modulators of ***,these neurological diseases occur in blood vessels,and the mechanisms are unclear by which neutrophil extracellular traps penetrate the blood-brain barrier to participate in immunothrombosis in traumatic brain *** review discusses the role of neutrophil extracellular traps in neuro-immunothrombosis and explores potential therapeutic interventions to modulate neutrophil extracellular traps that may reduce immunothrombosis and improve traumatic brain injury outcomes.

关键词： inflammation neuro-immunothrombosis neurologic diseases neurotrauma neutrophil extracellular traps platelet thrombosis traumatic brain injury

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Cognitive impairment after traumatic brain injury is associated with reduced long-term depression of excitatory postsynaptic potential in the rat hippocampal dentate gyrus

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Neural regeneration Research 2018年第10期13卷 1753-1758页

作者： Bao-Liang Zhang Yue-Shan Fan Ji-Wei Wang Zi-Wei Zhou Yin-Gang Wu Meng-Chen Yang Dong-Dong Sun Jian-Ning Zhang Department of neurosurgery Tianjin Medical University General HospitalTianjin Neurological InstituteKey Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous SystemMinistry of EducationTianjin Key Laboratory of InjuriesVariations and Regeneration of Nervous SystemTianjin China

traumatic brain injury can cause loss of neuronal tissue, remote symptomatic epilepsy, and cognitive deficits. However, the mechanisms underlying the effects of traumatic brain injury are not yet clear. Hippocampal excitability is strongly correlated with cognitive dysfunction and remote symptomatic epilepsy. In this study, we examined the relationship between traumatic brain injury-induced neuronal loss and subsequent hippocampal regional excitability. We used hydraulic percussion to generate a rat model of traumatic brain injury. At 7 days after injury, the mean modified neurological severity score was 9.5, suggesting that the neurological function of the rats was remarkably impaired. Electrophysiology and immunocytochemical staining revealed increases in the slope of excitatory postsynaptic potentials and long-term depression（indicating weakened long-term inhibition）, and the numbers of cholecystokinin and parvalbumin immunoreactive cells were clearly reduced in the rat hippocampal dentate gyrus. These results indicate that interneuronal loss and changes in excitability occurred in the hippocampal dentate gyrus. Thus, traumatic brain injury-induced loss of interneurons appears to be associated with reduced long-term depression in the hippocampal dentate gyrus.

关键词： nerve regeneration long-term depression traumatic brain injury hippocampus interneurons excitability dentate gyrus parvalbumin cholecystokinin electrophysiology quantification neural regeneration

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Multimodality management for chronic subdural hematoma in China: protocol and characteristics of an ambidirectional, nationwide, multicenter registry study

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中华神经外科杂志(英文) 2024年第2期10卷 1-10页

作者： Liu Tao Zhao Zhihao Huang Jinhao Zhu Xide Chen Weiliang Lin Kun Yu Yunhu Li Zhanying Fan Yibing Liu Mingqi Nie Meng Liu Xuanhui Gao Chuang Quan Wei Qian Yu Wu Chenrui Yuan Jiangyuan Wu Di Lv Chuanxiang Dong Shiying Mi Liang Tian Yu Tian Ye Zhang Jianning Jiang Rongcai Department of neurosurgery Tianjin Medical University General Hospital Tianjin China Ministry of Education Tianjin Neurological Institute Key Laboratory of Post Neuro-injury Neuro-repair and Regeneration in Central Nervous System Tianjin Medical University General Hospital Tianjin China Department of neurosurgery Linyi People’s Hospital Shandong China Department of neurosurgery Haining People’s Hospital Zhejiang China Department of neurosurgery Fujian Provincial Hospital Fujian China Department of Clinical Research Center for neurological Disease the People’s Hospital of HongHuaGang District of ZunYi Guizhou China Department of neurosurgery Kailuan General Hospital Hebei China Department of neurosurgery Tianjin First Central Hospital Tianjin China Department of neurosurgery The First Hospital of Jilin University Changchun China

Background Despite its prevalence, there is ongoing debate regarding the optimal management strategy for chronic subdural hematoma (CSDH), reflecting the variability in clinical presentation and treatment outcomes. This ambidirectional, nationwide, multicenter registry study aims to assess the efficacy and safety of multimodality treatment approaches for CSDH in the Chinese ***/design A multicenter cohort of CSDH patients from 59 participating hospitals in mainland China was enrolled in this study. The treatment modalities encompassed a range of options and baseline demographics, clinical characteristics, radiographic findings, and surgical techniques were documented. Clinical outcomes, including hematoma resolution, recurrence rates, neurological status, and complications, were assessed at regular intervals during treatment, 3 months, 6 months, 1 year, and 2 years *** Between March 2022 and August 2023, a comprehensive cohort comprising 2173 individuals who met the criterion was assembled across 59 participating clinical sites. Of those patients, 81.1% were male, exhibiting an average age of 70.12 ± 14.53 years. A historical record of trauma was documented in 48.0% of cases, while headache constituted the predominant clinical presentation in 58.1% of patients. The foremost surgical modality employed was the burr hole (61.3%), with conservative management accounting for 25.6% of cases. Notably, a favorable clinical prognosis was observed in 88.9% of CSDH patients at 3 months, and the recurrence rate was found to be 2.4%.Conclusion This registry study provides critical insights into the multimodality treatment of CSDH in China, offering a foundation for advancing clinical practices, optimizing patient management, and ultimately, improving the quality of life for individuals suffering from this challenging neurosurgical *** registration ChiCTR2200057179

关键词： Chronic subdural hematoma Multimodality therapy Outcome Recurrence

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Hydroxysafflor yellow A improves learning and memory in a rat model of vascular dementia by increasing VEGF and NR1 in the hippocampus

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neuroscience Bulletin 2014年第3期30卷 417-424页

作者： Nan Zhang Mengya Xing Yiyi Wang Hao Liang Zhuo Yang Fudong Shi Yan Cheng Department of neurology Tianjin Medical University General Hospital Tianjin neurological Institute key laboratory of post-traumatic neuro-repair and regeneration in the central nervous system Ministry of Education Tianjin key laboratory of Injuries Variations and Regeneration of the Nervous System Tianjin Haihe Hospital Nankai University

Hydroxysafflor yellow A （HSYA） has angiogenesis- regulating and neuro-protective effects, but its effects on vascular dementia （VaD） are unknown. In this study, 30 adult Sprague-Dawley rats were. randomly allocated to five groups： normal, sham-operation, VaD alone （bilateral carotid artery occlusion）, VaD plus saline （control）, and VaD plus HSYA. One week after operation, the HSYA group received one daily tail-vein injection of 0.6 mg/100 g HSYA for two weeks. Five weeks after operation, the spatial memory of all five groups was evaluated by the water maze task, and synaptic plasticity in the hippocampus was assessed by the long-term potentiation （LTP） method. Vascular endothelial growth factor （VEGF） and N-methyi-D- aspartic acid receptor 1 （NR1） expression in the hippocampus was detected via Western blot. We found that, compared with the group with VaD alone, the group with HSYA had a reduced escape latency in the water maze （P 〈0.05）, and the LTP at CA3- CA1 synapses in the hippocampus was enhanced （P 〈0.05）. Western blot in the late-phase VaD group showed slight up-regulation of VEGF and down- regulation of NR1 in the hippocampus, while HSYA significantly up-regulated both VEGF and NRI. These results suggested that HSYA promotes angiogenesis and increases synaptic plasticity, thus improving spatial learning and memory in the rat model of VaD.

关键词： vascular dementia hydroxysafflor yellow A long-term potentiation NMDA receptor vascular endothelial growth factor

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Expert opinion on translational research for advanced glioblastoma treatment

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Cancer Biology & Medicine 2023年第5期20卷 344-352页

作者： Xiaoteng Cui Yunfei Wang Junhu Zhou Qixue Wang Chunsheng Kang laboratory of neuro-oncology Tianjin Neurological InstituteKey Laboratory of Post-Neuro Injury Neuro-Repair and Regeneration in Central Nervous SystemMinistry of Education and Tianjin CityTianjin Medical University General HospitalTianjin 300052China

Malignant gliomas are known to be one of the most difficult diseases to diagnose and treat because of the infiltrative growth pattern,rapid progression,and poor *** antitumor drugs are not ideal for the treatment of gliomas due to the blood-brain ***(TMZ)is a DNA alkylating agent that can cross the blood-brain *** the only first-line chemotherapeutic drug for malignant gliomas at present,TMZ is widely utilized to provide a survival benefit;however,some patients are inherently insensitive to *** addition,patients could develop acquired resistance during TMZ treatment,which limits antitumor *** clarify the mechanism underlying TMZ resistance,numerous studies have provided multilevel solutions,such as improving the effective concentration of TMZ in tumors and developing novel small molecule *** review discusses the in-depth mechanisms underlying TMZ drug resistance,thus aiming to provide possibilities for the establishment of personalized therapeutic strategies against malignant gliomas and the accelerated development and transformation of new targeted drugs.

关键词： Malignant gliomas glioblastoma temozolomide chemoresistance small molecule drugs

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High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

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Neural regeneration Research 2025年第9期20卷 2611-2623页

作者： Mengshi Yang Miao Bai Yuan Zhuang Shenghua Lu Qianqian Ge Hao Li Yu Deng Hongbin Wu Xiaojian Xu Fei Niu Xinlong Dong Bin Zhang Baiyun Liu Beijing Tiantan Hospital Capital Medical UniversityBeijingChina Department of neurology The First Hospital of Tsinghua UniversityBeijingChina Department of neurotrauma and Beijing key laboratory of central nervous system Injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of Critical Care Medicine Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Center for Nerve Injury and repair Beijing Institute of Brain DisordersChina National Clinical Research Center for Neurological DiseasesBeijingChina

Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury,the fundamental regulatory and functional mechanisms remain insufficiently *** potent anti-inflammato ry agents,the use of glucoco rticoids in traumatic brain injury is still controversial,and their regulatory effects on microglial polarization are not yet *** the present study,we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of *** vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial ***,dexamethasone,RU486(a glucocorticoid receptor antagonist),and ruxolitinib(a Janus kinase 1 antagonist)were ***-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of *** Morris water maze,quantitative reverse transcription-polymerase chain reaction,western blotting,immunofluorescence and confocal microscopy analysis,and TUNEL,Nissl,and Golgi staining were performed to investigate our ***-throughput sequencing results showed that arginase 1,a marker of M2 microglia,was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at3 days post-traumatic brain *** dexamethasone inhibited M1 and M2 microglia,with a more pronounced inhibitory effect on M2microglia in vitro and in *** receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain ***,glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death,and also decreased the density of dendritic spines.A possible downstream receptor signaling mechanism is th

关键词： apoptosis BV2 microglia dexamethasone glucocorticoid receptor glucocorticoids innate immune system microglial polarization neuroinflammation primary microglia traumatic brain injury

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Mechanisms underlying the promotion of functional recovery by deferoxamine after spinal cord injury in rats

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Neural regeneration Research 2017年第6期12卷 959-968页

作者： Jian Hao Bo Li Hui-quan Duan Chen-xi Zhao Yan Zhang Chao Sun Bin Pan Chang Liu Xiao-hong Kong Xue Yao Shi-qing Feng Department of Orthopedics Tianjin Medical University General Hospital School of Medicine Nankai University Tianjin neurological Institute Key Laboratory of Post-Neuroinjury Neuro-Repair and Regeneration in Central Nervous System Ministry of Education

Deferoxamine, a clinically safe drug used for treating iron overload, also repairs spinal cord injury although the mechanism for this action remains unknown. Here, we determined whether deferoxamine was therapeutic in a rat model of spinal cord injury and explored potential mechanisms for this effect. Spinal cord injury was induced by impacting the spinal cord at the thoracic T10 vertebra level. One group of injured rats received deferoxamine, a second injured group received saline, and a third group was sham operated. Both 2 days and 2 weeks after spinal cord injury, total iron ion levels and protein expression levels of the proinflammatory cytokines tumor necrosis factor-α and interleukin-1β and the pro-apoptotic protein caspase-3 in the spinal cords of the injured deferoxamine-treated rats were significantly lower than those in the injured saline-treated group. The percentage of the area positive for glial fibrillary acidic protein immunoreactivity and the number of terminal deoxynucleotidyl transferase d UTP nick end labeling-positive cells were also significantly decreased both 2 days and 2 weeks post injury, while the number of Neu N-positive cells and the percentage of the area positive for the oligodendrocyte marker CNPase were increased in the injured deferoxamine-treated rats. At 14–56 days post injury, hind limb motor function in the deferoxamine-treated rats was superior to that in the saline-treated rats. These results suggest that deferoxamine decreases total iron ion, tumor necrosis factor-α, interleukin-1β, and caspase-3 expression levels after spinal cord injury and inhibits apoptosis and glial scar formation to promote motor function recovery.

关键词： injured interleukin glial caspase saline underlying fibrillary minutes acidic neuronal

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Decreased numbers of circulating endothelial progenitor cells are associated with hyperglycemia in patients with traumatic brain injury

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Neural regeneration Research 2019年第6期14卷 984-990页

作者： Hui-Jie Wei Li Liu Fang-Lian Chen Dong Wang Liang Wang Zeng-Guang Wang Rong-Cai Jiang Jing-Fei Dong Jie-Li Chen Jian-Ning Zhang Department of neurosurgery Tianjin Medical University General HospitalTianjin Neurological InstituteKey Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous SystemMinistry of EducationTianjin Key Laboratory of InjuriesVariations and Regeneration of Nervous System Department of neurosurgery Peking University International Hospital Thrombosis Research Section Department of MedicineBaylor College of Medicine Department of neurology Henry Ford Health System

Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their ***, the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear. In this study, 101 traumatic brain injury patients admitted to the Department of neurosurgery, Tianjin Medical University General Hospital or the Department of neurosurgery, Tianjin Huanhu Hospital, China, were enrolled from April 2005 to March 2007. The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1, 4, 7, 14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis, respectively. The number of circulating endothelial progenitor cells and blood sugar levels in 37 healthy control subjects were also examined. Compared with controls, the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury, and then increased at 4 days after injury,and reached a peak at 7 days after injury. Compared with controls, blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable. At 1, 4, and 7 days after injury, the number of circulating endothelial progenitor cells was negatively correlated with blood sugar levels(r =-0.147, P traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells. This study was approved by the Ethical Committee of Tianjin Medical University General Hospital, China(approval No. 200501) in January 2015.

关键词： nerve regeneration endothelial progenitor cells vascular repair vascular remodeling angiogenesis neovascularization blood glucose hyperglycemia traumatic brain injury mobilization suppression senescence alternative therapy brain damage neural regeneration

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Dynamic changes in growth factor levels over a 7-day period predict the functional outcomes of traumatic brain injury

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Neural regeneration Research 2018年第12期13卷 2134-2140页

作者： Shuai Zhou Dong-Pei Yin Yi Wang Ye Tian Zeng-Guang Wang Jian-Ning Zhang Department of Intensive Care Unit Tianjin Medical University General Hospital Tianjin China Tianjin neurological Institute Tianjin China key laboratory of post-trauma neuro-repair and regeneration in central nervous system Ministry of Education Tianjin China Tianjin key laboratory of Injuries Variations and Regeneration of Nervous System Tianjin China Department of neurosurgery Tianjin Medical University General Hospital Tianjin China

traumatic brain injury（TBI） can result in poor functional outcomes and death, and overall outcomes are varied. Growth factors, such as angiopoietin-1（Ang-1）, vascular endothelial growth factor（VEGF）, and granulocyte-colony stimulating factor（G-CSF）, play important roles in the neurological functions. This study investigated the relationship between serum growth factor levels and long-term outcomes after TBI. Blood samples from 55 patients were collected at 1, 3 and 7 days after TBI. Blood samples from 39 healthy controls were collected as a control group. Serum Ang-1, G-CSF, and VEGF levels were measured using ELISA. Patients were monitored for 3 months using the Glasgow Outcome Scale-Extended（GOSE）. Patients having a GOSE score of 〉 5 at 3 months were categorized as a good outcome, and patients with a GOSE score of 1-5 were categorized as a bad outcome. Our data demonstrated that TBI patients showed significantly increased growth factor levels within 7 days compared with healthy controls. Serum levels of Ang-1 at 1 and 7 days and G-CSF levels at 7 days were significantly higher in patients with good outcomes than in patients with poor outcomes. VEGF levels at 7 days were remarkably higher in patients with poor outcomes than in patients with good outcomes. Receiver operating characteristic analysis showed that the best cut-off points of serum growth factor levels at 7 days to predict functional outcome were 1,333 pg/mL for VEGF, 447.2 pg/mL for G-CSF, and 90.6 ng/mL for Ang-1. These data suggest that patients with elevated levels of serum Ang-1, G-CSF, and decreased VEGF levels had a better prognosis in the acute phase of TBI（within 7 days）. This study was registered with the Chinese Clinical Trial Registry（registration number： ChiCTR1800018251） on September 7, 2018.

关键词： nerve regeneration traumatic brain injury vascular endothelial growth factor angiopoietin-1 granulocyte-colony stimulating factor outcomes secondary brain injuries blood-brain barrier brain edema acute phase clinical trial neural regeneration

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Stability of rat models of fluid percussion-induced traumatic brain injury: comparison of three different impact forces

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Neural regeneration Research 2015年第7期10卷 1088-1094页

作者： Yun-peng Lin Rong-cai Jiang Jian-ning Zhang Department of neurosurgery Tianjin Medical University General Hospital Tianjin neurological Institute key laboratory of post-trauma neurorepair and regeneration in central nervous system Ministry of Education Tianjin key laboratory of Injuries Variations and Regeneration of Nervous System Tianjin Medical University General Hospital

Fluid percussion-induced traumatic brain injury models have been widely used in experimental research for years. In an experiment, the stability of impaction is inevitably affected by factors such as the appearance of liquid spikes. Management of impact pressure is a crucial factor that determines the stability of these models, and direction of impact control is another basic element. To improve experimental stability, we calculated a pressure curve by generating repeated impacts using a fluid percussion device at different pendulum angles. A stereotactic frame was used to control the direction of impact. We produced stable and reproducible models, including mild, moderate, and severe traumatic brain injury, using the MODEL01-B device at pendulum angles of 6°, 11° and 13°, with corresponding impact force values of 1.0 ± 0.11 atm（101.32 ± 11.16 k Pa）, 2.6 ± 0.16 atm（263.44 ± 16.21 k Pa）, and 3.6 ± 0.16 atm（364.77 ± 16.21 k Pa）, respectively. Behavioral tests, hematoxylin-eosin staining, and magnetic resonance imaging revealed that models for different degrees of injury were consistent with the clinical properties of mild, moderate, and severe craniocerebral injuries. Using this method, we established fluid percussion models for different degrees of injury and stabilized pathological features based on precise power and direction control.

关键词： nerve regeneration traumatic brain injury fluid percussion impact force pressure curve head fixed impact peak animal models neural regeneration

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