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Pro-and anti-epileptic roles of microglia 认领
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作者 Shinichi Kinoshita Ryuta Koyama 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1369-1371,共3页
Microglia are brain-resident immune cells that contribute to the maintenance of brain homeostasis.In the epileptic brain, microglia show various activation phenotypes depending on the stage of epileptogenesis.Therefor... Microglia are brain-resident immune cells that contribute to the maintenance of brain homeostasis.In the epileptic brain, microglia show various activation phenotypes depending on the stage of epileptogenesis.Therefore, it remains unclear whether microglial activation acts in a pro-epileptic or anti-epileptic manner.In mesial temporal lobe epilepsy, one of the most common form of epilepsies, microglia exhibit at least two distinct morphologies, amoeboid shape and ramified shape.Amoeboid microglia are often found in sclerotic area, whereas ramified microglia are mainly found in non-sclerotic area;however, it remains unclear whether these structurally distinct microglia share separate roles in the epileptic brain.Here, we review the roles of the two distinct microglial phenotypes, focusing on their pro-and anti-epileptic roles in terms of inflammatory response, regulation of neurogenesis and microglia-neuron interaction. 展开更多
关键词 EPILEPSY EPILEPTOGENESIS inflammatory cytokines MICROGLIA NEUROGENESIS neuron-microglia interaction SEIZURE
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The therapeutic potential of targeting exchange protein directly activated by cyclic adenosine 3',5'-monophosphate(Epac)for central nervous system trauma 认领
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作者 Alba Guijarro-Belmar Dominik Mateusz Domanski +2 位作者 Xuenong Bo Derryck Shewan Wenlong Huang 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期460-469,共10页
Millions of people worldwide are affected by traumatic spinal cord injury,which usually results in permanent sensorimotor disability.Damage to the spinal cord leads to a series of detrimental events including ischaemi... Millions of people worldwide are affected by traumatic spinal cord injury,which usually results in permanent sensorimotor disability.Damage to the spinal cord leads to a series of detrimental events including ischaemia,haemorrhage and neuroinflammation,which over time result in further neural tissue loss.Eventually,at chronic stages of traumatic spinal cord injury,the formation of a glial scar,cystic cavitation and the presence of numerous inhibitory molecules act as physical and chemical barriers to axonal regrowth.This is further hindered by a lack of intrinsic regrowth ability of adult neurons in the central nervous system.The intracellular signalling molecule,cyclic adenosine 3′,5′-monophosphate(cAMP),is known to play many important roles in the central nervous system,and elevating its levels as shown to improve axonal regeneration outcomes following traumatic spinal cord injury in animal models.However,therapies directly targeting cAMP have not found their way into the clinic,as cAMP is ubiquitously present in all cell types and its manipulation may have additional deleterious effects.A downstream effector of cAMP,exchange protein directly activated by cAMP 2(Epac2),is mainly expressed in the adult central nervous system,and its activation has been shown to mediate the positive effects of cAMP on axonal guidance and regeneration.Recently,using ex vivo modelling of traumatic spinal cord injury,Epac2 activation was found to profoundly modulate the post-lesion environment,such as decreasing the activation of astrocytes and microglia.Pilot data with Epac2 activation also suggested functional improvement assessed by in vivo models of traumatic spinal cord injury.Therefore,targeting Epac2 in traumatic spinal cord injury could represent a novel strategy in traumatic spinal cord injury repair,and future work is needed to fully establish its therapeutic potential. 展开更多
关键词 ASTROCYTES axonal regeneration cAMP central nervous system regeneration Epac glial scar microglia NEUROINFLAMMATION neurons spinal cord spinal cord injury traumatic spinal cord injury
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Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury 认领
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作者 Ulrich Goebel Stefanie Scheid +4 位作者 Sashko Spassov Nils Schallner Jakob Wollborn Hartmut Buerkle Felix Ulbrich 《中国神经再生研究:英文版》 SCIE CAS 2021年第1期192-198,共7页
We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STA... We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STAT3)and nuclear factor kappa B(NF-κB)are also affected by argon and may play a role in neuroprotection.It also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain inflammation.Despite intensive research,the further exact mechanism remains unclear.In this study,human neuroblastoma cells were damaged in vitro with rotenone over a period of 4 hours(to mimic cerebral ischemia and reperfusion damage),followed by a 2-hour post-conditioning with argon(75%).In a separate in vivo experiment,retinal ischemia/reperfusion injury was induced in rats by increasing intraocular pressure for 1 hour.Upon reperfusion,argon was administered by inhalation for 2 hours.Argon reduced the binding of the transcription factors signal transducer and activator of transcription 3,nuclear factor kappa B,activator protein 1,and nuclear factor erythroid 2-related factor 2,which are involved in regulation of neuronal damage.Flow cytometry analysis showed that argon downregulated the Fas ligand.Some transcription factors were regulated by toll-like receptors;therefore,their effects could be eliminated,at least in part,by the TLR2 and TLR4 inhibitor oxidized phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine(OxPAPC).Argon treatment reduced microglial activation after retinal ischemia/reperfusion injury.Subsequent quantitative polymerase chain reaction analysis revealed a reduction in the pro-inflammatory cytokines interleukin(IL-1α),IL-1β,IL-6,tumor necrosis factorα,and inducible nitric oxide synthase.Our results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial activation.Argon has no known side effects o 展开更多
关键词 ARGON ischemia/reperfusion injury MICROGLIA NEUROINFLAMMATION NEUROPROTECTION noble gas SH-SY5Y toll-like receptor transcription factor
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TP53-induced glycolysis and apoptosis regulator alleviates hypoxia/ischemia-induced microglial pyroptosis and ischemic brain damage 认领
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作者 Lan-Lan Tan Xiao-Lu Jiang +8 位作者 Li-Xiao Xu Gen Li Chen-Xi Feng Xin Ding Bin Sun Zheng-Hong Qin Zu-Bin Zhang Xing Feng Mei Li 《中国神经再生研究:英文版》 SCIE CAS 2021年第6期1037-1043,共7页
Our previous studies have demonstrated that TP53-induced glycolysis and apoptosis regulator(TIGAR)can protect neurons after cerebral ischemia/reperfusion.However,the role of TIGAR in neonatal hypoxic-ischemic brain da... Our previous studies have demonstrated that TP53-induced glycolysis and apoptosis regulator(TIGAR)can protect neurons after cerebral ischemia/reperfusion.However,the role of TIGAR in neonatal hypoxic-ischemic brain damage(HIBD)remains unknown.In the present study,7-day-old Sprague-Dawley rat models of HIBD were established by permanent occlusion of the left common carotid artery followed by 2-hour hypoxia.At 6 days before induction of HIBD,a lentiviral vector containing short hairpin RNA of either TIGAR or gasdermin D(LV-sh_TIGAR or LV-sh_GSDMD)was injected into the left lateral ventricle and striatum.Highly aggressively proliferating immortalized(HAPI)microglial cell models of in vitro HIBD were established by 2-hour oxygen/glucose deprivation followed by 24-hour reoxygenation.Three days before in vitro HIBD induction,HAPI microglial cells were transfected with LV-sh_TIGAR or LV-sh_GSDMD.Our results showed that TIGAR expression was increased in the neonatal rat cortex after HIBD and in HAPI microglial cells after oxygen/glucose deprivation/reoxygenation.Lentivirusmediated TIGAR knockdown in rats markedly worsened pyroptosis and brain damage after hypoxia/ischemia in vivo and in vitro.Application of exogenous nicotinamide adenine dinucleotide phosphate(NADPH)increased the NADPH level and the glutathione/oxidized glutathione ratio and decreased reactive oxygen species levels in HAPI microglial cells after oxygen/glucose deprivation/reoxygenation.Additionally,exogenous NADPH blocked the effects of TIGAR knockdown in neonatal HIBD in vivo and in vitro.These findings show that TIGAR can inhibit microglial pyroptosis and play a protective role in neonatal HIBD.The study was approved by the Animal Ethics Committee of Soochow University of China(approval No.2017LW003)in 2017. 展开更多
关键词 hypoxic-ischemic brain damage in vitro in vivo MICROGLIA NADPH PYROPTOSIS ROS TIGAR
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The Yin-Yang of osteopontin in nervous system diseases: damage versus repair 认领
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作者 Giuseppe Cappellano Domizia Vecchio +7 位作者 Luca Magistrelli Nausicaa Clemente Davide Raineri Camilla Barbero Mazzucca Eleonora Virgilio Umberto Dianzani Annalisa Chiocchetti Cristoforo Comi 《中国神经再生研究:英文版》 SCIE CAS 2021年第6期1131-1137,共7页
Osteopontin is a broadly expressed pleiotropic protein,and is attracting increased attention because of its role in the pathophysiology of several inflammatory,degenerative,autoimmune,and oncologic diseases.In fact,in... Osteopontin is a broadly expressed pleiotropic protein,and is attracting increased attention because of its role in the pathophysiology of several inflammatory,degenerative,autoimmune,and oncologic diseases.In fact,in the last decade,several studies have shown that osteopontin contributes to tissue damage not only by recruiting harmful inflammatory cells to the site of lesion,but also increasing their survival.The detrimental role of osteopontin has been indeed well documented in the context of different neurological conditions(i.e.,multiple sclerosis,Parkinson’s,and Alzheimer’s diseases).Intriguingly,recent findings show that osteopontin is involved not only in promoting tissue damage(the Yin),but also in repair/regenerative mechanisms(the Yang),mostly triggered by the inflammatory response.These two apparently discordant roles are partly related to the presence of different functional domains in the osteopontin molecule,which are exposed after thrombin or metalloproteases cleavages.Such functional domains may in turn activate intracellular signaling pathways and mediate cell-cell and cell-matrix interactions.This review describes the current knowledge on the Yin and Yang features of osteopontin in nervous system diseases.Understanding the mechanisms behind the Yin/Yang would be relevant to develop highly specific tools targeting this multifunctional protein. 展开更多
关键词 Alzheimer’s disease cytokine immunity MICROGLIA multiple sclerosis NEUROINFLAMMATION neuroprotection NEUROTOXICITY Parkinson’s disease Spp1 stroke
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The phenotypic convergence between microglia and peripheral macrophages during development and neuroinflammation paves the way for new therapeutic perspectives 认领
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作者 Francesca Grassivaro Gianvito Martino Cinthia Farina 《中国神经再生研究:英文版》 SCIE CAS 2021年第4期635-637,共3页
Microglia,the tissue resident macrophages of the brain,are increasingly recognized as key players for central nervous system development and homeostasis.They are long-lived cells deriving from a transient wave of yolk... Microglia,the tissue resident macrophages of the brain,are increasingly recognized as key players for central nervous system development and homeostasis.They are long-lived cells deriving from a transient wave of yolk-sac derived erythro-myeloid progenitors early in development.Their unique ontology has prompted the search for specific markers to be used for their selective investigation and manipulation.The first generation of genomewide expression studies has provided a bundle of transcripts(such as Olfml3,Fcrls,Tmem119,P2ry12,Gpr34,and Siglech)useful to distinguish microglia from peripheral macrophages.However,more recent reports have revealed that microglial phenotype is constantly shaped by the microenvironment in a time-,and context-dependent manner.In this article,we review data that provide additional pieces to this complex scenario and show the existence of unexpected phenotypic convergence between microglia and peripheral macrophages at certain developmental stages and under pathological conditions.These observations suggest that the two cell types act synergically boosting their mutual activities depending on the microenvironment.This novel information about the biology of microglia and peripheral macrophages sheds new light about their therapeutic potential for neuroinflammatory and neurodegenerative diseases. 展开更多
关键词 cell reprogramming cell therapy MACROPHAGES MICROGLIA NEUROINFLAMMATION PLASTICITY
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Hydroxyethylstarch revisited for acute brain injury treatment 认领
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作者 Martin A.Schick Malgorzata Burek +3 位作者 Carola Y.Förster Michiaki Nagai Christian Wunder Winfried Neuhaus 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1372-1376,共5页
Infusion of the colloid hydroxyethylstarch has been used for volume substitution to maintain hemodynamics and microcirculation after e.g., severe blood loss.In the last decade it was revealed that hydroxyethylstarch c... Infusion of the colloid hydroxyethylstarch has been used for volume substitution to maintain hemodynamics and microcirculation after e.g., severe blood loss.In the last decade it was revealed that hydroxyethylstarch can aggravate acute kidney injury, especially in septic patients.Because of the serious risk for critically ill patients, the administration of hydroxyethylstarch was restricted for clinical use.Animal studies and recently published in vitro experiments showed that hydroxyethylstarch might exert protective effects on the blood-brain barrier.Since the prevention of blood-brain barrier disruption was shown to go along with the reduction of brain damage after several kinds of insults, we revisit the topic hydroxyethylstarch and discuss a possible niche for the application of hydroxyethylstarch in acute brain injury treatment. 展开更多
关键词 acute subarachnoid hemorrhage ASTROCYTE chronic kidney disease delayed cerebral ischemia MICROGLIA neurovascular unit osmotic pressure PERICYTE STROKE traumatic brain injury
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Regulation of neuroimmune processes by damage-and resolution-associated molecular patterns 认领
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作者 Andis Klegeris 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期423-429,共7页
Sterile inflammatory processes are essential for the maintenance of central nervous system homeostasis,but they also contribute to various neurological disorders,including neurotrauma,stroke,and demyelinating or neuro... Sterile inflammatory processes are essential for the maintenance of central nervous system homeostasis,but they also contribute to various neurological disorders,including neurotrauma,stroke,and demyelinating or neurodegenerative diseases.Immune mechanisms in the central nervous system and periphery are regulated by a diverse group of endogenous proteins,which can be broadly divided into the pro-inflammatory damageassociated molecular patterns(DAMPs)and anti-inflammatory resolution-associated molecular patterns(RAMPs),even though there is notable overlap between the DAMPand RAMP-like activities for some of these molecules.Both groups of molecular patterns were initially described in peripheral immune processes and pathologies;however,it is now evident that at least some,if not all,of these immunomodulators also regulate neuroimmune processes and contribute to neuroinflammation in diverse central nervous system disorders.The review of recent literature demonstrates that studies on DAMPs and RAMPs of the central nervous system still lag behind the much broader research effort focused on their peripheral counterparts.Nevertheless,this review also reveals that over the last five years,significant advances have been made in our understanding of the neuroimmune functions of several well-established DAMPs,including high-mobility group box 1 protein and interleukin 33.Novel neuroimmune functions have been demonstrated for other DAMPs that previously were considered almost exclusively as peripheral immune regulators;they include mitochondrial transcription factor A and cytochrome C.RAMPs of the central nervous system are an emerging area of neuroimmunology with very high translational potential since some of these molecules have already been used in preclinical and clinical studies as candidate therapeutic agents for inflammatory conditions,such as multiple sclerosis and rheumatoid arthritis.The therapeutic potential of DAMP antagonists and neutralizing antibodies in central nervous system neuroinflammatory diseases is al 展开更多
关键词 Alzheimer's disease astrocytes DAMPS HMGB1 microglia neurodegeneration neuroimmune responses NEUROINFLAMMATION NEUROTRAUMA OLIGODENDROCYTES pattern-recognition receptors RAMPS
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Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models 认领
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作者 Shelly A.Cruz Zhaohong Qin +2 位作者 Konrad M.Ricke Alexandre F.R.Stewart Hsiao-Huei Chen 《中国神经再生研究:英文版》 SCIE CAS 2021年第1期129-136,共8页
Ischemic brain injury causes neuronal death and inflammation.Inflammation activates protein-tyrosine phosphatase 1B(PTP1B).Here,we tested the significance of PTP1B activation in glutamatergic projection neurons on fun... Ischemic brain injury causes neuronal death and inflammation.Inflammation activates protein-tyrosine phosphatase 1B(PTP1B).Here,we tested the significance of PTP1B activation in glutamatergic projection neurons on functional recovery in two models of stroke:by photothrombosis,focal ischemic lesions were induced in the sensorimotor cortex(SM stroke)or in the peri-prefrontal cortex(peri-PFC stroke).Elevated PTP1B expression was detected at 4 days and up to 6 weeks after stroke.While ablation of PTP1B in neurons of neuronal knockout(NKO)mice had no effect on the volume or resorption of ischemic lesions,markedly different effects on functional recovery were observed.SM stroke caused severe sensory and motor deficits(adhesive removal test)in wild type and NKO mice at 4 days,but NKO mice showed drastically improved sensory and motor functional recovery at 8 days.In addition,peri-PFC stroke caused anxiety-like behaviors(elevated plus maze and open field tests),and depression-like behaviors(forced swimming and tail suspension tests)in wild type mice 9 and 28 days after stroke,respectively,with minimal effect on sensory and motor function.Peri-PFC stroke-induced affective disorders were associated with fewer active(FosB+)neurons in the PFC and nucleus accumbens but more FosB+neurons in the basolateral amygdala,compared to sham-operated mice.In contrast,mice with neuronal ablation of PTP1B were protected from anxiety-like and depression-like behaviors and showed no change in FosB+neurons after peri-PFC stroke.Taken together,our study identifies neuronal PTP1B as a key component that hinders sensory and motor functional recovery and also contributes to the development of anxiety-like and depression-like behaviors after stroke.Thus,PTP1B may represent a novel therapeutic target to improve stroke recovery.All procedures for animal use were approved by the Animal Care and Use Committee of the University of Ottawa Animal Care and Veterinary Service(protocol 1806)on July 27,2018. 展开更多
关键词 adhesive removal test ANXIETY depression elevated plus maze forced swimming test Iba1 INTERLEUKIN-1Β MICROGLIA open field test tail suspension test tumor necrosis factor-α
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Ninjurin-1: a biomarker for reflecting the process of neuroinflammation after spinal cord injury 认领
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作者 Poornima D.E.Weerasinghe-Mudiyanselage Jeongtae Kim +3 位作者 Yuna Choi Changjong Moon Taekyun Shin Meejung Ahn 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1331-1335,共5页
Previous studies have shown that Ninjurin-1 participates in cell trafficking and axonal growth following central and peripheral nervous system neuroinflammation.But its precise roles in these processes and involvement... Previous studies have shown that Ninjurin-1 participates in cell trafficking and axonal growth following central and peripheral nervous system neuroinflammation.But its precise roles in these processes and involvement in spinal cord injury pathophysiology remain unclear.Western blot assay revealed that Ninjurin-1 levels in rats with spinal cord injury exhibited an upregulation until day 4 post-injury and slightly decreased thereafter compared with sham controls.Immunohistochemistry analysis revealed that Ninjurin-1 immunoreactivity in rats with spinal cord injury sharply increased on days 1 and 4 post-injury and slightly decreased on days 7 and 21 post-injury compared with sham controls.Ninjurin-1 immunostaining was weak in vascular endothelial cells, ependymal cells, and some glial cells in sham controls while it was relatively strong in macrophages, microglia, and reactive astrocytes.These findings suggest that a variety of cells, including vascular endothelial cells, macrophages, and microglia, secrete Ninjurin-1 and they participate in the pathophysiology of compression-induced spinal cord injury.All experimental procedures were approved by the Care and Use of Laboratory Animals of Jeju National University(approval No.2018-0029) on July 6, 2018. 展开更多
关键词 ASTROCYTES clip compression injury MACROPHAGE MICROGLIA NEUROINFLAMMATION Ninjurin-1 rat spinal cord
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Impact of pediatric traumatic brain injury on hippocampal neurogenesis 认领
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作者 Mariam Rizk Justin Vu Zhi Zhang 《中国神经再生研究:英文版》 SCIE CAS 2021年第5期926-933,共8页
Traumatic brain injury(TBI)is a major cause of mortality and morbidity in the pediatric population.With advances in medical care,the mortality rate of pediatric TBI has declined.However,more children and adolescents a... Traumatic brain injury(TBI)is a major cause of mortality and morbidity in the pediatric population.With advances in medical care,the mortality rate of pediatric TBI has declined.However,more children and adolescents are living with TBI-related cognitive and emotional impairments,which negatively affects the quality of their life.Adult hippocampal neurogenesis plays an important role in cognition and mood regulation.Alterations in adult hippocampal neurogenesis are associated with a variety of neurological and neurodegenerative diseases,including TBI.Promoting endogenous hippocampal neurogenesis after TBI merits significant attention.However,TBI affects the function of neural stem/progenitor cells in the dentate gyrus of hippocampus,which results in aberrant migration and impaired dendrite development of adult-born neurons.Therefore,a better understanding of adult hippocampal neurogenesis after TBI can facilitate a more successful neuro-restoration of damage in immature brains.Secondary injuries,such as neuroinflammation and oxidative stress,exert a significant impact on hippocampal neurogenesis.Currently,a variety of therapeutic approaches have been proposed for ameliorating secondary TBI injuries.In this review,we discuss the uniqueness of pediatric TBI,adult hippocampal neurogenesis after pediatric TBI,and current efforts that promote neuroprotection to the developing brains,which can be leveraged to facilitate neuroregeneration. 展开更多
关键词 adult hippocampal neurogenesis ASTROCYTES development MICROGLIA NEUROINFLAMMATION NEUROREGENERATION oxidative stress pediatric traumatic brain injury PLASTICITY stem cell
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丁酸钠抑制氟中毒可诱导小胶质细胞活化及炎症因子表达增多 认领
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作者 王正东 黄娜 +6 位作者 陈婧娴 郑作兵 胡鑫宇 李梅 苏晓 苏学森 颜南 《中国组织工程研究》 CAS 北大核心 2021年第7期1075-1080,共6页
背景:在中枢神经系统疾病中,致病因素刺激小胶质细胞过度活化分泌炎性因子继而导致神经元进一步损伤,去乙酰化酶抑制剂丁酸钠能否降低氟中毒引起小胶质细胞的过度活化以及引起的炎性作用,值得深入研究。目的:丁酸钠对氟诱导的小胶质细... 背景:在中枢神经系统疾病中,致病因素刺激小胶质细胞过度活化分泌炎性因子继而导致神经元进一步损伤,去乙酰化酶抑制剂丁酸钠能否降低氟中毒引起小胶质细胞的过度活化以及引起的炎性作用,值得深入研究。目的:丁酸钠对氟诱导的小胶质细胞过度活化以及炎性因子白细胞介素1β、白细胞介素6、肿瘤坏死因子α表达的影响。方法:用含体积分数为10%胎牛血清的DMEM/F12培养基常规培养BV-2小胶质细胞,取对数生长期细胞用CCK-8法观察不同浓度氟化钠、丁酸钠及二者联合使用对BV-2细胞活力的影响。通过倒置显微镜、RT-qPCR和Western blot法观察氟化钠、丁酸钠及二者联合应用后的BV-2细胞形态以及炎症因子白细胞介素1β、白细胞介素6、肿瘤坏死因子αmRNA和蛋白表达。结果与结论:①CCK-8结果:质量分数25×10^-6氟化钠能降低BV-2细胞活力,0.25 mmol/L丁酸钠能升高BV-2细胞活力;0.25 mmol/L丁酸钠能逆转25×10^-6氟化钠对BV-2细胞活力的降低作用;②RT-qPCR和western blot结果:0.25 mmol/L丁酸钠能够拮抗25×10^-6氟化钠引起的白细胞介素1β、白细胞介素6、肿瘤坏死因子α过表达作用;③结果说明在一定的剂量范围内,丁酸钠可减轻氟致小胶质细胞介导的炎症反应。 展开更多
关键词 干细胞 氟中毒 丁酸钠 氟化钠 小胶质细胞 炎症 因子 实验
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小胶质细胞介导神经元损伤在神经退行性疾病中的作用 认领
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作者 谢文佳 夏天娇 +2 位作者 周卿云 刘羽佳 顾小萍 《中国组织工程研究》 CAS 北大核心 2021年第7期1109-1115,共7页
背景:小胶质细胞是中枢神经系统驻留免疫细胞,具有感知、管家和防御功能。神经退行性疾病状态下,小胶质细胞功能紊乱导致或加重神经元损伤。目的:探讨神经退行性疾病中小胶质细胞介导的神经元损伤机制。方法:由第一作者以“microglia,ne... 背景:小胶质细胞是中枢神经系统驻留免疫细胞,具有感知、管家和防御功能。神经退行性疾病状态下,小胶质细胞功能紊乱导致或加重神经元损伤。目的:探讨神经退行性疾病中小胶质细胞介导的神经元损伤机制。方法:由第一作者以“microglia,neurodegenerative diseases,neuronal injury”为英文检索词,“小胶质细胞,神经退行性疾病,神经元损伤”为中文检索词,检索PubMed、中国知网、万方、维普等中英文数据库2001年1月至2020年1月发表的相关文献。结果与结论:神经退行性疾病中,小胶质细胞受到毒性物质干扰而感知过度导致激活增多,伴随管家功能亢进和强烈的神经炎症,造成神经元损伤;或因特定基因突变而出现感知和管家功能减弱,使毒性物质累积加重防御功能的失调,诱导神经元凋亡或坏死。探索神经退行性疾病中小胶质细胞介导的神经元损伤机制,可为神经退行性疾病的治疗提供多个靶点。 展开更多
关键词 干细胞 小胶质细胞 神经退行性疾病 神经元损伤 神经炎症 阿尔茨海默病 中枢神经系统 神经元死亡 综述
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Lycium barbarum polysaccharide-glycoprotein preventative treatment ameliorates aversive stimuli-induced depression 认领
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作者 Yun-Wei Fu Yan-Fang Peng +7 位作者 Xiao-Dan Huang Yan Yang Lu Huang Yue Xi Zheng-Fang Hu Song Lin Kwok-Fai So Chao-Ran Ren 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期543-549,共7页
Previous studies have shown that Lycium barbarum polysaccharide,the main active component of Lycium barbarum,exhibits antiinflammatory and antioxidant effects in treating neurological diseases.However,the therapeutic ... Previous studies have shown that Lycium barbarum polysaccharide,the main active component of Lycium barbarum,exhibits antiinflammatory and antioxidant effects in treating neurological diseases.However,the therapeutic action of Lycium barbarum polysaccharide on depression has not been studied.In this investigation,we established mouse models of depression using aversive stimuli including exposure to fox urine,air puff and foot shock and physical restraint.Concurrently,we administered 5 mg/kg per day Lycium barbarum polysaccharide-glycoprotein to each mouse intragastrically for the 28 days.Our results showed that long-term exposure to aversive stimuli significantly enhanced depressive-like behavior evaluated by the sucrose preference test and the forced swimming test and increased anxietylike behaviors evaluated using the open field test.In addition,aversive stimuli-induced depressed mice exhibited aberrant neuronal activity in the lateral habenula.Importantly,concurrent Lycium barbarum polysaccharide-glycoprotein treatment significantly reduced these changes.These findings suggest that Lycium barbarum polysaccharide-glycoprotein is a potential preventative intervention for depression and may act by preventing aberrant neuronal activity and microglial activation in the lateral habenula.The study was approved by the Jinan University Institutional Animal Care and Use Committee(approval No.20170301003)on March 1,2017. 展开更多
关键词 aversive stimuli behaviors DEPRESSION immune response inflammation lateral habenula Lycium barbarum polysaccharide mice MICROGLIA NEURON
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Dysfunctional glia:contributors to neurodegenerative disorders 认领
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作者 Marta Sidoryk-Węgrzynowicz Lidia Strużyńska 《中国神经再生研究:英文版》 SCIE CAS 2021年第2期218-222,共5页
Astrocytes are integral components of the central nervous system,where they are involved in numerous functions critical for neuronal development and functioning,including maintenance of blood-brain barrier,formation o... Astrocytes are integral components of the central nervous system,where they are involved in numerous functions critical for neuronal development and functioning,including maintenance of blood-brain barrier,formation of synapses,supporting neurons with nutrients and trophic factors,and protecting them from injury.These roles are markedly affected in the course of chronic neurodegenerative disorders,often before the onset of the disease.In this review,we summarize the recent findings supporting the hypothesis that astrocytes play a fundamental role in the processes contributing to neurodegeneration.We focus onα-synucleinopathies and tauopathies as the most common neurodegenerative diseases.The mechanisms implicated in the development and progression of these disorders appear not to be exclusively neuronal,but are often related to the astrocytic-neuronal integrity and the response of astrocytes to the altered microglial function.A profound understanding of the multifaceted functions of astrocytes and identification of their communication pathways with neurons and microglia in health and in the disease is of critical significance for the development of novel mechanism-based therapies against neurodegenerative disorders. 展开更多
关键词 astrocytes microglia NEURODEGENERATION NEUROINFLAMMATION synaptic dysfunction SYNUCLEINOPATHIES TAUOPATHIES
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Guanosine-5'-triphosphate cyclohydrolase 1 regulated long noncoding RNAs are potential targets for microglial activation in neuropathic pain 认领
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作者 Yan-Hu Liang Guo-Wu Chen +2 位作者 Xue-Song Li Shu Jia Chun-Yang Meng 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期596-600,共5页
Several studies have confirmed that microglia are involved in neuropathic pain.Inhibition of guanosine-5′-triphosphate cyclohydrolase 1(GTPCH1)can reduce the inflammation of microglia.However,the precise mechanism by... Several studies have confirmed that microglia are involved in neuropathic pain.Inhibition of guanosine-5′-triphosphate cyclohydrolase 1(GTPCH1)can reduce the inflammation of microglia.However,the precise mechanism by which GTPCH1 regulates neuropathic pain remains unclear.In this study,BV2 microglia were transfected with adenovirus to knockdown GTPCH1 expression.High throughput sequencing analysis revealed that the mitogen-activated protein kinase(MAPK)related pathways and proteins were the most significantly downregulated molecular function.Co-expression network analysis of Mapk14 mRNA and five long noncoding RNAs(lnc RNAs)revealed their correlation.Quantitative reverse transcription-polymerase chain reaction revealed that among five lnc RNAs,ENSMUST00000205634,ENSMUST00000218450 and ENSMUST00000156079 were related to the downregulation of Mapk14 mRNA expression.These provide some new potential targets for the involvement of GTPCH1 in neuropathic pain.This study is the first to note the differential expression of lnc RNAs and mRNA in GTPCH1 knockdown BV2 microglia.Findings from this study reveal the mechanism by which GTPCH1 activates microglia and provide new potential targets for microglial activation in neuropathic pain. 展开更多
关键词 cells factors INFLAMMATION MICROGLIA PAIN pathway protein RNA
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Microglia in neurodegenerative diseases 认领
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作者 Yu Xu Ming-Zhu Jin +1 位作者 Ze-Yong Yang Wei-Lin Jin 《中国神经再生研究:英文版》 SCIE CAS 2021年第2期270-280,共11页
A major feature of neurodegeneration is disruption of central nervous system homeostasis,during which microglia play diverse roles.In the central nervous system,microglia serve as the first line of immune defense and ... A major feature of neurodegeneration is disruption of central nervous system homeostasis,during which microglia play diverse roles.In the central nervous system,microglia serve as the first line of immune defense and function in synapse pruning,injury repair,homeostasis maintenance,and regulation of brain development through scavenging and phagocytosis.Under pathological conditions or various stimulations,microglia proliferate,aggregate,and undergo a variety of changes in cell morphology,immunophenotype,and function.This review presents the features of microglia,especially their diversity and ability to change dynamically,and reinterprets their role as sensors for multiple stimulations and as effectors for brain aging and neurodegeneration.This review also summarizes some therapeutic approaches for neurodegenerative diseases that target microglia. 展开更多
关键词 central nervous system MICROGLIA NEURODEGENERATION NEUROINFLAMMATION PLASTICITY
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前扣带回皮质中趋化因子CCL21参与模型大鼠的慢性病理性疼痛 认领
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作者 支亦博 章洁 +1 位作者 刘健 李伟彦 《中国组织工程研究》 CAS 北大核心 2021年第2期242-246,共5页
背景:慢性病理性疼痛目前形成机制尚不明确,有研究认为脊髓损伤后CCL21可以激活中枢神经中的小胶质细胞,且仅在受损的神经元中表达,促进慢性病理性疼痛的形成。目的:探讨大鼠眶下神经结扎后,前扣带回皮质是否参与慢性病理性疼痛的形成,... 背景:慢性病理性疼痛目前形成机制尚不明确,有研究认为脊髓损伤后CCL21可以激活中枢神经中的小胶质细胞,且仅在受损的神经元中表达,促进慢性病理性疼痛的形成。目的:探讨大鼠眶下神经结扎后,前扣带回皮质是否参与慢性病理性疼痛的形成,阻断前扣带回皮质中趋化因子CCL21是否可以减轻疼痛的发生。方法:雄性SD大鼠80只随机分成4组,每组20只。假手术组仅暴露大鼠眶下神经;模型组结扎大鼠左侧眶下神经;CCL21中和抗体组造模术后第7天于大鼠前扣带回皮质给予CCL21中和抗体;PBS组造模术后第7天于大鼠前扣带回皮质给予PBS溶液。假手术组及模型组大鼠分别于术后第3,5,7,14天开展行为学测试,CCL21中和抗体组及PBS组于给药后6 h进行行为学测试。所有大鼠行为学测试后麻醉处死,并取前扣带回皮质组织,采用Western Blot及免疫荧光法测定其中CCL21蛋白含量。结果与结论:①模型组大鼠术后痛阈较假手术组低,且前扣带回皮质中CCL21表达水平明显高于假手术组;②给予CCL21中和抗体之后,可看到CCL21表达有所降低,相对应大鼠痛阈也有相应的提升;③提示大鼠前扣带回皮质可能参与了慢性病理性疼痛的产生,且给予CCL21中和抗体可以改善疼痛。 展开更多
关键词 慢性疼痛 病理性 眶下神经结扎 前扣带回皮质 小胶质细胞 趋化因子 CCL21
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Microglial activation and adult neurogenesis after brain stroke 认领
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作者 Ijair R.C.dos Santos Michelle Nerissa C.Dias Walace Gomes-Leal 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期456-459,共4页
The discovery that new neurons are produced in some regions of the adult mammalian brain is a paradigm-shift in neuroscience research.These new-born cells are produced from neuroprogenitors mainly in the subventricula... The discovery that new neurons are produced in some regions of the adult mammalian brain is a paradigm-shift in neuroscience research.These new-born cells are produced from neuroprogenitors mainly in the subventricular zone at the margin of the lateral ventricle,subgranular zone in the hippocampal dentate gyrus and in the striatum,a component of the basal ganglia,even in humans.In the human hippocampus,neuroblasts are produced even in elderlies.The regulation of adult neurogenesis is a complex phenomenon involving a multitude of molecules,neurotransmitters and soluble factors released by different sources including glial cells.Microglia,the resident macrophages of the central nervous system,are considered to play an important role on the regulation of adult neurogenesis both in physiological and pathological conditions.Following stroke and other acute neural disorders,there is an increase in the numbers of neuroblast production in the neurogenic niches.Microglial activation is believed to display both beneficial and detrimental role on adult neurogenesis after stroke,depending on the activation level and brain location.In this article,we review the scientific evidence addressing the role of microglial activation on adult neurogenesis after ischemia.A comprehensive understanding of the microglial role after stroke and other neural disorders it is an important step for development of future therapies based on manipulation of adult neurogenesis. 展开更多
关键词 adult neurogenesis HIPPOCAMPUS ISCHEMIA MICROGLIA NEUROINFLAMMATION NEUROPROTECTION STROKE subventricular zone therapy
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疾病相关小胶质细胞在阿尔兹海默症发病中的作用研究 认领
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作者 崔雨沙 路欣 李峰 《中国比较医学杂志》 CAS 北大核心 2020年第5期132-136,共5页
作为大脑固有免疫细胞,小胶质细胞在阿尔兹海默症(Alzheimer’s disease,AD)的发病过程中发挥着不可替代的作用。过去的研究一直使用传统M1、M2分型来解释小胶质细胞的功能,但随着技术的发展,我们现在可以从细胞转录组学或基因组学、蛋... 作为大脑固有免疫细胞,小胶质细胞在阿尔兹海默症(Alzheimer’s disease,AD)的发病过程中发挥着不可替代的作用。过去的研究一直使用传统M1、M2分型来解释小胶质细胞的功能,但随着技术的发展,我们现在可以从细胞转录组学或基因组学、蛋白组学等方面来更加全面地认识小胶质细胞,而不是仅仅靠几个标志基因来对小胶质细胞进行分型。疾病相关的小胶质细胞(disease associated microglia,DAM)就是从细胞转录组学的角度建立的小胶质细胞亚型,这一亚型的确立对于构建小胶质细胞新的分型意义重大,并且预测了许多新的AD危险位点,对于下一步研究至关重要。 展开更多
关键词 阿尔兹海默症 小胶质细胞 疾病相关小胶质细胞
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