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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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Activation of adult endogenous neurogenesis by a hyaluronic acid collagen gel containing basic fibroblast growth factor promotes remodeling and functional recovery of the injured cerebral cortex

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Neural Regeneration Research 2025年第10期20卷 2923-2937页

作者： Yan Li Peng Hao Hongmei Duan Fei Hao Wen Zhao Yudan Gao Zhaoyang Yang Kwok-Fai So Xiaoguang Li department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina China Rehabilitation Science Institute China Rehabilitation Research CenterBeijing Key Laboratory of Neural Injury and RehabilitationBeijingChina Center of Neural injury and Repair Beijing Institute for Brain DisordersBeijingChina beijing key laboratory for Biomaterials and Neural Regeneration School of Engineering MedicineBeihang UniversityBeijingChina Guangdong-HongKong-Macao Institute of CNS Regeneration Ministry of Education CNS Regeneration Collaborative Joint LaboratoryJinan UniversityGuangzhouGuangdong ProvinceChina Bioland laboratory(Guangzhou Regenerative Medicine and Health Guangdong laboratory) GuangzhouGuangdong ProvinceChina department of Ophthalmology and State key laboratory of Brain and Cognitive Sciences The University of Hong KongHong Kong Special Administration RegionChina Center for Brain Science and Brain-Inspired Intelligence Guangdong-HongKong-Macao Greater Bay AreaGuangzhouGuangdong ProvinceChina Co-innovation Center of Neuroregeneration Nantong UniversityNantongJiangsu ProvinceChina department of Biomedical Engineering School of Biological Science and Medical EngineeringBeihang UniversityBeijingChina

The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after ***,whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions,such as the cortex,remains *** this study,we implanted a hyaluronic acid collagen gel loaded with basic fibroblast growth factor into the motor cortex immediately following traumatic *** findings reveal that this gel effectively stimulated the proliferation and migration of endogenous neural stem/progenitor cells,as well as their differentiation into mature and functionally integrated ***,these new neurons reconstructed the architecture of cortical layers II to VI,integrated into the existing neural circuitry,and ultimately led to improved brain *** findings offer novel insight into potential clinical treatments for traumatic cerebral cortex injuries.

关键词： adult endogenous neurogenesis basic fibroblast growth factor-hyaluronic acid collagen gel cortical remodeling functional recovery migration motor cortex injury neural circuits neural stem cells newborn neurons proliferation

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Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury

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Neural Regeneration Research 2023年第5期18卷 1046-1051页

作者： Xiao-Jian Xu Qian-Qian Ge Meng-Shi Yang Yuan Zhuang Bin Zhang Jin-Qian Dong Fei Niu Hao Li Bai-Yun Liu beijing key laboratory of central nervous system injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina beijing key laboratory of central nervous system injury and department of Neurosurgery Beijing Neurosurgical Institute and Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Nerve injury and Repair Center of beijing Institute for Brain Disorders BeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

After brain injury, infiltration and abnormal activation of neutrophils damages brain tissue and worsens inflammation, but the mediators that connect activated neutrophils with neuroinflammation have not yet been fully clarified. To identify regulators of neutrophil-mediated neuroinflammation after traumatic brain injury, a mouse model of traumatic brain injury was established by controlled cortical impact. At 7 days post-injury(sub-acute phase), genome-wide transcriptomic data showed that interleukin 17 A-associated signaling pathways were markedly upregulated, suggesting that interleukin 17 A may be involved in neuroinflammation. Double immunofluorescence staining showed that interleukin 17 A was largely secreted by neutrophils rather than by glial cells and neurons. Furthermore, nuclear factor-kappaB and Stat3, both of which are important effectors in interleukin 17 A-mediated proinflammatory responses, were significantly activated. Collectively, our findings suggest that neutrophil-derived interleukin 17 A participates in neutrophil-mediated neuroinflammation during the subacute phase of traumatic brain injury. Therefore, interleukin 17 A may be a promising therapeutic target for traumatic brain injury.

关键词： immune infiltration innate immunity interleukin-17A neurodegenerative disease neuroinflammation neutrophils secondary brain injury transcription factor transcriptome traumatic brain injury

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Comparative transcriptomic analysis of rat versus mouse cerebral cortex after traumatic brain injury

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Neural Regeneration Research 2021年第7期16卷 1235-1243页

作者： Meng-Shi Yang Xiao-Jian Xu Bin Zhang Fei Niu Bai-Yun Liu beijing key laboratory of central nervous system injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina beijing key laboratory of central nervous system injury and department of Neurosurgery Beijing Neurosurgical Institute and Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Nerve injury and Repair Center of beijing Institute for Brain Disorders BeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

The heterogeneity of traumatic brain injury(TBI)-induced secondary injury has greatly hampered the development of effective treatments for TBI *** common processes across species may be an innovative strategy to combat debilitating *** the present study, a cross-species transcriptome comparison was performed for the first time to determine the fundamental processes of secondary brain injury in Sprague-Dawley rat and C57/BL6 mouse models of TBI, caused by acute controlled cortical *** RNA sequencing data from the mouse model of TBI were downloaded from the Gene Expression Omnibus(ID: GSE79441) at the National Center for Biotechnology *** the rat data, peri-injury cerebral cortex samples were collected for transcriptomic analysis 24 hours after *** expressed gene-based functional analysis revealed that common features between the two species were mainly involved in the regulation and activation of the innate immune response, including complement cascades as well as Toll-like and nucleotide oligomerization domain-like receptor *** findings were further corroborated by gene set enrichment ***, transcription factor analysis revealed that the families of signal transducers and activators of transcription(STAT), basic leucine zipper(BZIP), Rel homology domain(RHD), and interferon regulatory factor(IRF) transcription factors play vital regulatory roles in the pathophysiological processes of TBI, and are also largely associated with *** findings suggest that targeting the common innate immune response might be a promising therapeutic approach for *** animal experimental procedures were approved by the beijing Neurosurgical Institute Animal Care and Use Committee(approval No.201802001) on June 6, 2018.

关键词： cognitive impairment cross-species comparison gene set enrichment analysis inflammation innate immune neurodegenerative disease secondary injury transcription factor transcriptome traumatic brain injury

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Genome-wide interrogation of transfer RNA-derived small RNAs in a mouse model of traumatic brain injury

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Neural Regeneration Research 2022年第2期17卷 386-394页

作者： Xiao-Jian Xu Meng-Shi Yang Bin Zhang Qian-Qian Ge Fei Niu Jin-Qian Dong Yuan Zhuang Bai-Yun Liu beijing key laboratory of central nervous system injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina beijing key laboratory of central nervous system injury and department of Neurosurgery Beijing Neurosurgical Institute and Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Nerve injury and Repair Center of beijing Institute for Brain Disorders BeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

Transfer RNA(t RNA)-derived small RNAs(ts RNAs) are a recently established family of regulatory small non-coding RNAs that modulate diverse biological processes. Growing evidence indicates that ts RNAs are involved in neurological disorders and play a role in the pathogenesis of neurodegenerative disease. However, whether ts RNAs are involved in traumatic brain injury-induced secondary injury remains poorly understood. In this study, a mouse controlled cortical impact model of traumatic brain injury was established, and integrated ts RNA and messenger RNA(m RNA) transcriptome sequencing were used. The results revealed that 103 ts RNAs were differentially expressed in the mouse model of traumatic brain injury at 72 hours, of which 56 ts RNAs were upregulated and 47 ts RNAs were downregulated. Based on micro RNA-like seed matching and Pearson correlation analysis, 57 differentially expressed ts RNA-m RNA interaction pairs were identified, including 29 ts RNAs and 26 m RNAs. Moreover, Gene Ontology annotation of target genes revealed that the significantly enriched terms were primarily associated with inflammation and synaptic function. Collectively, our findings suggest that ts RNAs may be associated with traumatic brain injury-induced secondary brain injury, and are thus a potential therapeutic target for traumatic brain injury. The study was approved by the beijing Neurosurgical Institute Animal Care and Use Committee(approval No. 20190411) on April 11, 2019.

关键词： gene set enrichment analysis inflammation integrated analysis neurodegenerative disease next-generation sequencing secondary injury synaptic function transfer RNA-derived small RNAs transfer RNAs traumatic brain injury

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The pivotal role of microglia in injury and the prognosis of subarachnoid hemorrhage

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Neural Regeneration Research 2025年第7期20卷 1829-1848页

作者： Wenjing Ning Shi Lv Qian Wang Yuzhen Xu department of Rehabilitation The Second Affiliated Hospital of Shandong First Medical UniversityTaianShandong ProvinceChina department of central laboratory The Affiliated Taian City Central Hospital of Qingdao UniversityTaianShandong ProvinceChina

Subarachnoid hemorrhage leads to a series of pathological changes,including vascular spasm,cellular apoptosis,blood–brain barrier damage,cerebral edema,and white matter ***,which are the key immune cells in the central nervous system,maintain homeostasis in the neural environment,support neurons,mediate apoptosis,participate in immune regulation,and have neuroprotective *** evidence has shown that microglia play a pivotal role in the pathogenesis of subarachnoid hemorrhage and affect the process of injury and the prognosis of subarachnoid ***,microglia play certain neuroprotective roles in the recovery phase of subarachnoid *** approaches aimed at modulating microglia function are believed to attenuate subarachnoid hemorrhage *** provides new targets and ideas for the treatment of subarachnoid ***,an in-depth and comprehensive summary of the role of microglia after subarachnoid hemorrhage is still *** review describes the activation of microglia after subarachnoid hemorrhage and their roles in the pathological processes of vasospasm,neuroinflammation,neuronal apoptosis,blood–brain barrier disruption,cerebral edema,and cerebral white matter *** also discusses the neuroprotective roles of microglia during recovery from subarachnoid hemorrhage and therapeutic advances aimed at modulating microglial function after subarachnoid ***,microglia in subarachnoid hemorrhage are targeted with TLR inhibitors,nuclear factor-κB and STAT3 pathway inhibitors,glycine/tyrosine kinases,NLRP3 signaling pathway inhibitors,Gasdermin D inhibitors,vincristine receptorαreceptor agonists,ferroptosis inhibitors,genetic modification techniques,stem cell therapies,and traditional Chinese ***,most of these are still being evaluated at the laboratory *** clinical studies and data on subarachnoid hemorrhage are required to improve the treatment of subarachnoid hemor

关键词： apoptosis blood–brain barrier brain edema microglia neuroinflammation neuron neuroprotection subarachnoid hemorrhage vasoconstriction white matter injury

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Protein profiling identified mitochondrial dysfunction and synaptic abnormalities after dexamethasone intervention in rats with traumatic brain injury

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Neural Regeneration Research 2021年第12期16卷 2438-2445页

作者： Fei Niu Bin Zhang Jie Feng Xiang Mao Xiao-Jian Xu Jin-Qian Dong Bai-Yun Liu department of neurotrauma Beijing Key Laboratory of Central Nervous System InjuryBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijingChina key laboratory of central nervous system injury Research Center for Brain TumorBeijing Institute of Brain DisordersBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina department of Neurosurgery the First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina Center for Nerve injury and Repair Beijing Institute of Brain DisordersBeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid *** to the latest guidelines for the treatment of traumatic brain injury in the United States,high-dose glucocorticoids cause neurological *** investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect,rat controlled cortical impact models of traumatic brain injury were *** 1 hour and 2 days after surgery,rat models were intraperitoneally administered dexamethasone 10 mg/*** results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone *** Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling *** blot analysis and immunohistochemistry results showed that Ndufv2,Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model *** findings suggest that dexamethasone may promote a compensatory increase in complex I subunits(Ndufs2 and Ndufv2),increase the expression of mitochondrial enzyme Maob,and upregulate synaptic-transmission-related protein *** changes may be caused by nerve injury after traumatic brain injury treatment by *** study was approved by Institutional Ethics Committee of beijing Neurosurgical Institute(approval No.201802001)on June 6,2018.

关键词： dexamethasone Gria3 Maob mass spectrometry mitochondrial dysfunction Ndufs2 Ndufv2 proteomics synaptic abnormalities traumatic brain injury

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Tandem Mass Tag-based proteomics analysis reveals the vital role of inflammation in traumatic brain injury in a mouse model

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Neural Regeneration Research 2023年第1期18卷 155-161页

作者： Jin-Qian Dong Qian-Qian Ge Sheng-Hua Lu Meng-Shi Yang Yuan Zhuang Bin Zhang Fei Niu Xiao-Jian Xu Bai-Yun Liu department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijingChina beijing key laboratory of central nervous system injury Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Center for Nerve injury and Repair Beijing Institute of Brain DisordersBeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

Proteomics is a powerful tool that can be used to elucidate the underlying mechanisms of diseases and identify new ***,it may also be helpful for understanding the detailed pathological mechanism of traumatic brain injury(TBI).In this study,we performed Tandem Mass Tag-based quantitative analysis of cortical proteome profiles in a mouse model of *** results showed that there were 302 differentially expressed proteins in TBI mice compared with normal mice 7 days after *** Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that these differentially expressed proteins were predominantly involved in inflammatory responses,including complement and coagulation cascades,as well as chemokine signaling *** transcription factor analysis revealed that the inflammation-related transcription factors NF-κB1,RelA,IRF1,STAT1,and Spi1 play pivotal roles in the secondary injury that occurs after TBI,which further corroborates the functional enrichment for inflammatory *** results suggest that inflammation-related proteins and inflammatory responses are promising targets for the treatment of TBI.

关键词： bioinformatics complement cascade mass spectrometry neuroinflammation proteomics secondary injury subacute phase tandem mass tag transcription factor 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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Neutrophil extracellular traps mediate neuro-immunothrombosis

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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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