检索结果-南通市图书馆

A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities

引用

Military Medical Research 2024年第2期11卷 228-267页

作者： Miguel A.Ortega Oscar Fraile-Martinez Cielo García-Montero Sergio Haro Miguel Ángel Álvarez-Mon Diego De Leon-Oliva Ana M.Gomez-Lahoz Jorge Monserrat Mar Atienza-Pérez David Díaz Elisa Lopez-Dolado Melchor Álvarez-Mon Department of Medicine and Medical Specialities University of Alcala28801 Alcala de HenaresSpain Ramón y Cajal Institute of Sanitary Research(IRYCIS) 28034 MadridSpain Department of Psychiatry and Mental Health Hospital Universitario Infanta Leonor28031 MadridSpain Service of Rehabilitation National Hospital for Paraplegic PatientsCarr.de la PeraledaS/N45004 ToledoSpain Immune System Diseases‑Rheumatology Service and Internal Medicine University Hospital Príncipe de Asturias(CIBEREHD)28806 Alcala de HenaresSpain

Spinal cord injury(SCI)is a devastating and disabling medical condition generally caused by a traumatic event(primary injury).This initial trauma is accompanied by a set of biological mechanisms directed to ameliorate neural damage but also exacerbate initial damage(secondary injury).The alterations that occur in the spinal cord have not only local but also systemic consequences and virtually all organs and tissues of the body incur important changes after SCI,explaining the progression and detrimental consequences related to this condition.Psychoneuroimmunoendocrinology(PNIE)is a growing area of research aiming to integrate and explore the interactions among the different systems that compose the human organism,considering the mind and the body as a whole.The initial traumatic event and the consequent neurological disruption trigger immune,endocrine,and multisystem dysfunction,which in turn affect the patient's psyche and well-being.In the present review,we will explore the most important local and systemic consequences of SCI from a PNIE perspective,defining the changes occurring in each system and how all these mechanisms are interconnected.Finally,potential clinical approaches derived from this knowledge will also be collectively presented with the aim to develop integrative therapies to maximize the clinical management of these patients.

关键词： Spinal cord injury(SCI) Psychoneuroimmunoendocrinology(PNIE) secondary injury Immunoinflammatory dysfunction Gut microbiota Translational opportunities

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

T cell interactions with microglia in immune-inflammatory processes of ischemic stroke

引用

Neural Regeneration Research 2025年第5期20卷 1277-1292页

作者： Yuxiao Zheng Zilin Ren Ying Liu Juntang Yan Congai Chen Yanhui He Yuyu Shi Fafeng Cheng Qingguo Wang Changxiang Li Xueqian Wang School of Traditional Chinese Medicine Beijing University of Chinese MedicineBeijingChina Library Beijing University of Chinese MedicineBeijingChina Dongzhimen Hospital Beijing University of Chinese MedicineBeijingChina

The primary mechanism of secondary injury after cerebral ischemia may be the brain inflammation that emerges after an ischemic stroke,which promotes neuronal death and inhibits nerve tissue regeneration.As the first immune cells to be activated after an ischemic stroke,microglia play an important immunomodulatory role in the progression of the condition.After an ischemic stroke,peripheral blood immune cells(mainly T cells)are recruited to the central nervous system by chemokines secreted by immune cells in the brain,where they interact with central nervous system cells(mainly microglia)to trigger a secondary neuroimmune response.This review summarizes the interactions between T cells and microglia in the immune-inflammatory processes of ischemic stroke.We found that,during ischemic stroke,T cells and microglia demonstrate a more pronounced synergistic effect.Th1,Th17,and M1 microglia can co-secrete proinflammatory factors,such as interferon-γ,tumor necrosis factor-α,and interleukin-1β,to promote neuroinflammation and exacerbate brain injury.Th2,Treg,and M2 microglia jointly secrete anti-inflammatory factors,such as interleukin-4,interleukin-10,and transforming growth factor-β,to inhibit the progression of neuroinflammation,as well as growth factors such as brain-derived neurotrophic factor to promote nerve regeneration and repair brain injury.Immune interactions between microglia and T cells influence the direction of the subsequent neuroinflammation,which in turn determines the prognosis of ischemic stroke patients.Clinical trials have been conducted on the ways to modulate the interactions between T cells and microglia toward anti-inflammatory communication using the immunosuppressant fingolimod or overdosing with Treg cells to promote neural tissue repair and reduce the damage caused by ischemic stroke.However,such studies have been relatively infrequent,and clinical experience is still insufficient.In summary,in ischemic stroke,T cell subsets and activated microglia act synergistically to regulate inflammator

关键词： brain immune inflammation interaction ischemic stroke mechanism microglia neuron secondary injury T cells

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

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

引用

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

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Photobiomodulation provides neuroprotection through regulating mitochondrial fission imbalance in the subacute phase of spinal cord injury

引用

Neural Regeneration Research 2023年第9期18卷 2005-2010页

作者： Xin Li Xuan-Kang Wang Zhi-Jie Zhu Zhuo-Wen Liang Peng-Hui Li Yang-Guang Ma Tan Ding Kun Li Xiao-Shuang Zuo Cheng Ju Zhi-Hao Zhang Zhi-Wen Song Hui-Lin Quan Jia-Wei Zhang Liang Luo Zhe Wang Xue-Yu Hu Department of Orthopedics Xijing HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina 2967 Hospital of People’s Liberation Army Joint Logistic Support Force DalianLiaoning ProvinceChina

Increasing evidence indicates that mitochonarial lission imbalance plays an important role in derayed neuronal cell death. Our previous study round that photo biomodulation improved the motor function of rats with spinal cord injury.However,the precise mechanism remains unclear.To investigate the effect of photo biomodulation on mitochondrial fission imbalance after spinal cord injury,in this study,we treated rat models of spinal co rd injury with 60-minute photo biomodulation(810 nm,150 mW) every day for 14 consecutive days.Transmission electron microscopy results confirmed the swollen and fragmented alte rations of mitochondrial morphology in neurons in acute(1 day) and subacute(7 and 14 days) phases.Photo biomodulation alleviated mitochondrial fission imbalance in spinal cord tissue in the subacute phase,reduced neuronal cell death,and improved rat posterior limb motor function in a time-dependent manner.These findings suggest that photobiomodulation targets neuronal mitochondria,alleviates mitochondrial fission imbalance-induced neuronal apoptosis,and thereby promotes the motor function recovery of rats with spinal cord injury.

关键词： low-level laser therapy mitochondria mitochondrial dynamics mitochondrial fission imbalance neuron photobiomodulation secondary injury spinal cord injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis

引用

Neural Regeneration Research 2022年第12期17卷 2702-2709页

作者： Yi-Xin Chen Talifu Zuliyaer Bin Liu Shuang Guo De-Gang Yang Feng Gao Yan Yu Ming-Liang Yang Liang-Jie Du Jian-Jun Li School of Rehabilitation Medicine Capital Medical UniversityBeijingChina China Rehabilitation Science Institute BeijingChina Center of Neural injury and Repair Beijing Institute for Brain DisordersBeijingChina Department of Spinal and Neural Functional Reconstruction China Rehabilitation Research CenterBeijingChina Beijing Key Laboratory of Neural injury and Rehabilitation BeijingChina Department of Rehabilitation Medicine Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina Department of Spine Surgery Hunan Provincial People’s Hospital(The First Affiliated Hospital of Hunan Normal University)ChangshaHunan ProvinceChina

Ferroptosis is a recently discovered form of iron-dependent cell death,which occurs during the pathological process of various central nervous system diseases or injuries,including secondary spinal cord injury.Selenium has been shown to promote neurological function recovery after cerebral hemorrhage by inhibiting ferroptosis.However,whether selenium can promote neurological function recovery after spinal cord injury as well as the underlying mechanism remain poorly understood.In this study,we injected sodium selenite(3μL,2.5μM)into the injury site of a rat model of T10 vertebral contusion injury 10 minutes after spinal cord injury modeling.We found that sodium selenite treatment greatly decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal.Furthermore,sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4,promoted the survival of neurons and oligodendrocytes,inhibited the proliferation of astrocytes,and promoted the recovery of locomotive function of rats with spinal cord injury.These findings suggest that sodium selenite can improve the locomotive function of rats with spinal cord injury possibly through the inhibition of ferroptosis via the specificity protein 1/glutathione peroxidase 4 pathway.

关键词： ferroptosis glutathione peroxidase 4 glutathione iron lipid peroxidation neural regeneration secondary injury sodium selenite specificity protein 1 spinal cord injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

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

引用

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 biomarkers.Therefore,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 TBI.Our results showed that there were 302 differentially expressed proteins in TBI mice compared with normal mice 7 days after injury.Gene 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 pathways.Subsequent 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 factors.Our 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

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Quantitative proteomic and phosphoproteomic analyses of the hippocampus reveal the involvement of NMDAR1 signaling in repetitive mild traumatic brain injury

引用

Neural Regeneration Research 2023年第12期18卷 2711-2719页

作者： Zhicheng Tian Zixuan Cao Erwan Yang Juan Li Dan Liao Fei Wang Taozhi Wang Zhuoyuan Zhang Haofuzi Zhang Xiaofan Jiang Xin Li Peng Luo Department of Neurosurgery Xijing HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina The Sixth Regiment School of Basic MedicineFourth Military Medical UniversityXi’anShaanxi ProvinceChina Department of Neurobiology School of Basic MedicineFourth Military Medical UniversityXi’anShaanxi ProvinceChina Medical Experiment Center Shaanxi University of Chinese MedicineXianyangShaanxi ProvinceChina Department of Anesthesiology The Second Hospital of Jilin UniversityJilin UniversityChangchunJilin ProvinceChina School of Life Science Northwest UniversityXi’anShaanxi ProvinceChina Department of Anesthesiology Xijing HospitalFourth Military Medical UniversityXi’anShaanxi ProvinceChina

The cumulative damage caused by repetitive mild traumatic brain injury can cause long-term neurodegeneration leading to cognitive impairment.This cognitive impairment is thought to result specifically from damage to the hippocampus.In this study,we detected cognitive impairment in mice 6 weeks after repetitive mild traumatic brain injury using the novel object recognition test and the Morris water maze test.Immunofluorescence staining showed that p-tau expression was increased in the hippocampus after repetitive mild traumatic brain injury.Golgi staining showed a significant decrease in the total density of neuronal dendritic spines in the hippocampus,as well as in the density of mature dendritic spines.To investigate the specific molecular mechanisms underlying cognitive impairment due to hippocampal damage,we performed proteomic and phosphoproteomic analyses of the hippocampus with and without repetitive mild traumatic brain injury.The differentially expressed proteins were mainly enriched in inflammation,immunity,and coagulation,suggesting that non-neuronal cells are involved in the pathological changes that occur in the hippocampus in the chronic stage after repetitive mild traumatic brain injury.In contrast,differentially expressed phosphorylated proteins were mainly enriched in pathways related to neuronal function and structure,which is more consistent with neurodegeneration.We identified N-methyl-D-aspartate receptor 1 as a hub molecule involved in the response to repetitive mild traumatic brain injury,and western blotting showed that,while N-methyl-D-aspartate receptor 1 expression was not altered in the hippocampus after repetitive mild traumatic brain injury,its phosphorylation level was significantly increased,which is consistent with the omics results.Administration of GRP78608,an N-methyl-D-aspartate receptor 1 antagonist,to the hippocampus markedly improved repetitive mild traumatic brain injury-induced cognitive impairment.In conclusion,our findings suggest that N-methyl-D-aspartate receptor 1 sig

关键词： cognitive impairment Grin1 hippocampus learning memory N-methyl-D-aspartate N-methyl-D-aspartate receptor 1 phosphoproteomic proteomic repetitive mild traumatic brain injury(rmTBI) secondary injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Alterations in gut microbiota are related to metabolite profiles in spinal cord injury

引用

Neural Regeneration Research 2023年第5期18卷 1076-1083页

作者： Jian-Ning Kang Zheng-Fang Sun Xin-Yu Li Xiao-Di Zhang Zheng-Xin Jin Ce Zhang Ying Zhang Hui-Yun Wang Na-Na Huang Jian-Hao Jiang Bin Ning Central Hospital Affiliated to Shandong First Medical University Shandong First Medical University&Shandong Academy of Medical SciencesJinanShandong ProvinceChina Department of Spinal Surgery Jinan Central HospitalCheeloo College of MedicineShandong UniversityJinanShandong ProvinceChina School of Clinical Medicine Weifang Medical UniversityWeifangShandong ProvinceChina Department of Traumatic Orthopedics Binzhou Medical University HospitalBinzhou Medical UniversityBinzhouShandong ProvinceChina

Studies have shown that gut microbiota metabolites can enter the central nervous system via the blood-spinal cord barrier and cause neuroinflammation, thus constituting secondary injury after spinal cord injury. To investigate the correlation between gut microbiota and metabolites and the possible mechanism underlying the effects of gut microbiota on secondary injury after spinal cord injury, in this study, we established mouse models of T8–T10 traumatic spinal cord injury. We used 16 S rRNA gene amplicon sequencing and metabolomics to reveal the changes in gut microbiota and metabolites in fecal samples from the mouse model. Results showed a severe gut microbiota disturbance after spinal cord injury, which included marked increases in pro-inflammatory bacteria, such as Shigella, Bacteroides, Rikenella, Staphylococcus, and Mucispirillum and decreases in anti-inflammatory bacteria, such as Lactobacillus, Allobaculum, and Sutterella. Meanwhile, we identified 27 metabolites that decreased and 320 metabolites that increased in the injured spinal cord. Combined with pathway enrichment analysis, five markedly differential amino acids(L-leucine, L-methionine, L-phenylalanine, L-isoleucine and L-valine) were screened out, which play a pivotal role in activating oxidative stress and inflammatory responses following spinal cord injury. Integrated correlation analysis indicated that the alteration of gut microbiota was related to the differences in amino acids, which suggests that disturbances in gut microbiota might participate in the secondary injury through the accumulation of partial metabolites that activate oxidative stress and inflammatory responses. Findings from this study provide a new theoretical basis for improving the secondary injury after spinal cord injury through fecal microbial transplantation.

关键词： 16S rRNA gene amplicon sequencing amino acid metabolism dysbacteriosis gut microbiota inflammation metabolic disturbance metabolites metabolomics secondary injury spinal cord injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Expression of yeast silencing information regulator 2 in secondary injury of intracerebral hemorrhage

引用

Journal of Translational Neuroscience 2021年第1期6卷 29-32页

作者： Na Hu Ran An Yanzhong Chang Department of Biochemistry Basic Medicine CollegeHebei University of Chinese MedicineShijiazhuang 050000China Heibei Key Laboratory of Chinese Medicine Research on Cardio-cerebrovascular Disease Shijiazhuang 050000China College of Life Sciences Hebei Normal UniversityShijiazhuang 050000China

Objective:to investigate the expression of yeast silencing information regulator 2(Sirt2)in the secondary injury of intracerebral hemorrhage(ICH).Methods:twelve Sprague Dawley(SD)rats were randomly divided into a sham group and an ICH group,with six rats in each group.A rat model of ICH was established by injecting collagenase type IV into the right striatum of the rats.The expression of Sirt2 was measured by Western blot and immunohistochemistry after ICH.Result:the behavioral score of the ICH rats was the lowest at 48 h after the operation;therefore the rats at 48 h after surgery were selected as the model rats.The expression of Sirt2 was significantly higher in the striatal tissue of the ICH rats compared with the sham group(P<0.05).Conclusion:the expression of Sirt2 around hematoma in ICH rats decreases,and Sirt2 is expected to become a new target for ICH treatment.

关键词： intracerebral hemorrhage(ICH) secondary injury silencing information regulator 2(Sirt2)

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Decoding epigenetic codes: new frontiers in exploring recovery from spinal cord injury

引用

Neural Regeneration Research 2020年第9期15卷 1613-1622页

作者： Bo-Yin Zhang Peng-Yu Chang Qing-San Zhu Yu-Hang Zhu Saijilafu Department of Orthopedic Surgery China-Japan Union Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of Radiotherapy The First Bethune Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of Orthopedics The First Affiliated Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina

Spinal cord injury that results in severe neurological disability is often incurable.The poor clinical outcome of spinal cord injury is mainly caused by the failure to reconstruct the injured neural circuits.Several intrinsic and extrinsic determinants contribute to this inability to reconnect.Epigenetic regulation acts as the driving force for multiple pathological and physiological processes in the central nervous system by modulating the expression of certain critical genes.Recent studies have demonstrated that post-SCI alteration of epigenetic landmarks is strongly associated with axon regeneration,glial activation and neurogenesis.These findings not only establish a theoretical foundation for further exploration of spinal cord injury,but also provide new avenues for the clinical treatment of spinal cord injury.This review focuses on the epigenetic regulation in axon regeneration and secondary spinal cord injury.Together,these discoveries are a selection of epigenetic-based prognosis biomarkers and attractive therapeutic targets in the treatment of spinal cord injury.

关键词： axon regeneration epigenetic biomarkers epigenetic modification histone microRNA prognosis secondary injury spinal cord injury

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：