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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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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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Astrocytes: a double-edged sword in neurodegenerative diseases 认领
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作者 Zhi-Bin Ding Li-Juan Song +3 位作者 Qing Wang Gajendra Kumar Yu-Qing Yan Cun-Gen Ma 《中国神经再生研究:英文版》 SCIE CAS 2021年第9期1702-1710,共9页
Astrocytes play multifaceted and vital roles in maintaining neurophysiological function of the central nervous system by regulating homeostasis, increasing synaptic plasticity, and sustaining neuroprotective effects. ... Astrocytes play multifaceted and vital roles in maintaining neurophysiological function of the central nervous system by regulating homeostasis, increasing synaptic plasticity, and sustaining neuroprotective effects. Astrocytes become activated as a result of inflammatory responses during the progression of pathological changes associated with neurodegenerative disorders. Reactive astrocytes(neurotoxic A1 and neuroprotective A2) are triggered during disease progression and pathogenesis due to neuroinflammation and ischemia. However, only a limited body of literature describes morphological and functional changes of astrocytes during the progression of neurodegenerative diseases. The present review investigated the detrimental and beneficial roles of astrocytes in neurodegenerative diseases reported in recent studies, as these cells have promising therapeutic potential and offer new approaches for treatment of neurodegenerative diseases. 展开更多
关键词 A1 A2 ASTROCYTES neurodegenerative diseases NEUROINFLAMMATION NEURON NEUROPROTECTION NEUROTOXICITY polarization REACTIVITY
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Neuroprotective and anti-inflammatory effects of a therapy combining agonists of nicotinic α7 and σ1 receptors in a rat model of Parkinson’s disease 认领
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作者 Steven Vetel Laura Foucault-Fruchard +6 位作者 Claire Tronel Frédéric Buron Jackie Vergote Sylvie Bodard Sylvain Routier Sophie Sérrière Sylvie Chalon 《中国神经再生研究:英文版》 SCIE CAS 2021年第6期1099-1104,共6页
To date there is no treatment able to stop or slow down the loss of dopaminergic neurons that characterizes Parkinson’s disease.It was recently observed in a rodent model of Alzheimer’s disease that the interaction ... To date there is no treatment able to stop or slow down the loss of dopaminergic neurons that characterizes Parkinson’s disease.It was recently observed in a rodent model of Alzheimer’s disease that the interaction between the α7 subtype of nicotinic acetylcholine receptor(α7-nAChR)and sigma-1 receptor(σ1-R)could exert neuroprotective effects through the modulation of neuroinflammation which is one of the key components of the pathophysiology of Parkinson’s disease.In this context,the aim of the present study was to assess the effects of the concomitant administration of N-(3R)-1-azabicyclo[2.2.2]oct-3-yl-furo[2,3-c]pyridine-5-carboxamide(PHA)543613 as an α7-nAChR agonist and 2-(4-morpholinethyl)1-phenylcyclohexanecarboxylate(PRE)-084 as aσ1-R agonist in a well-characterized 6-hydroxydopamine rat model of Parkinson’s disease.The animals received either vehicle separately or the dual therapy PHA/PRE once a day until day 14 postlesion.Although no effect was noticed in the amphetamine-induced rotation test,our data has shown that the PHA/PRE treatment induced partial protection of the dopaminergic neurons(15-20%),assessed by the dopamine transporter density in the striatum and immunoreactive tyrosine hydroxylase in the substantia nigra.Furthermore,this dual therapy reduced the degree of glial activation consecutive to the 6-hydroxydopamine lesion,i.e,the 18 kDa translocation protein density and glial fibrillary acidic protein staining in the striatum,and the CD11b and glial fibrillary acidic protein staining in the substantia nigra.Hence,this study reports for the first time that concomitant activation of α7-nAChR andσ1-R can provide a partial recovery of the nigro-striatal dopaminergic neurons through the modulation of microglial activation.The study was approved by the Regional Ethics Committee(CEEA Val de Loire n°19)validated this protocol(Authorization N°00434.02)on May 15,2014. 展开更多
关键词 6-HYDROXYDOPAMINE astrocytes microglial activation neurodegeneration neuroinflammation nicotinicα7 receptor Parkinson’s disease PHA 543613 PRE-084 sigma-1 receptor
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银耳多糖超声波提取工艺优化及抗BV2细胞炎症的作用研究 认领
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作者 谢玲娜 韩萍 杜志云 《广东工业大学学报》 CAS 2021年第2期94-98,共5页
以银耳为原料,采用超声波辅助热水浸提法提取银耳多糖,以多糖提取率为指标,以超声波功率、提取料液比、提取温度和提取时间为影响因素,设计单因素试验,并通过正交试验得到较佳提取工艺。通过用TRPV1(Transient Receptor Potential Vanil... 以银耳为原料,采用超声波辅助热水浸提法提取银耳多糖,以多糖提取率为指标,以超声波功率、提取料液比、提取温度和提取时间为影响因素,设计单因素试验,并通过正交试验得到较佳提取工艺。通过用TRPV1(Transient Receptor Potential Vanilloid1)试剂盒检测了小胶质细胞TRPV1的释放水平,与脂多糖(Lipopolysaccharide,LPS)对照组相比,不同质量浓度的银耳多糖组(62.5,250,1000μg/mL)均能不同程度地抑制TRPV1的释放量。说明了银耳多糖对于BV2小胶质细胞炎症具有良好的抑制作用。 展开更多
关键词 银耳多糖 超声波 热水浸提 正交试验 神经炎症 辣椒素受体1
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慢性脑低灌注致认知障碍的神经炎症机制 认领
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作者 赵耀 付剑亮 《医学综述》 2021年第2期220-225,共6页
慢性脑低灌注(CCH)是血管性痴呆的危险因素之一,其相关机制涉及氧化应激、自噬、炎症反应等多个方面,其中神经炎症贯穿于CCH所致动物认知障碍的病理变化过程。被激活的小胶质细胞和其他神经胶质细胞产生大量的炎症因子,参与神经元损伤... 慢性脑低灌注(CCH)是血管性痴呆的危险因素之一,其相关机制涉及氧化应激、自噬、炎症反应等多个方面,其中神经炎症贯穿于CCH所致动物认知障碍的病理变化过程。被激活的小胶质细胞和其他神经胶质细胞产生大量的炎症因子,参与神经元损伤、脑白质病变、海马区损伤和β-淀粉样蛋白沉积等,这些损伤最终导致认知障碍的发生发展。深入研究CCH中神经炎症的意义以及小胶质细胞的促炎或抑炎作用,可为CCH引起的认知障碍提供新的治疗思路。 展开更多
关键词 慢性脑低灌注 神经炎症 小胶质细胞 白质病变 认知障碍
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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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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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Dynamic glial response and crosstalk in demyelination-remyelination and neurodegeneration processes 认领
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作者 Tianci Chu Lisa B.E.Shields +5 位作者 Wenxin Zeng Yi Ping Zhang Yuanyi Wang Gregory N.Barnes Christopher B.Shields Jun Cai 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1359-1368,共10页
Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system.It is characterized by blood-brain barrier dysfunction throughout the course of multiple s... Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system.It is characterized by blood-brain barrier dysfunction throughout the course of multiple sclerosis, followed by the entry of immune cells and activation of local microglia and astrocytes.Glial cells(microglia, astrocytes, and oligodendrocyte lineage cells) are known as the important mediators of neuroinflammation, all of which play major roles in the pathogenesis of multiple sclerosis.Network communications between glial cells affect the activities of oligodendrocyte lineage cells and influence the demyelination-remyelination process.A finely balanced glial response may create a favorable lesion environment for efficient remyelination and neuroregeneration.This review focuses on glial response and neurodegeneration based on the findings from multiple sclerosis and major rodent demyelination models.In particular, glial interaction and molecular crosstalk are discussed to provide insights into the potential cell-and molecule-specific therapeutic targets to improve remyelination and neuroregeneration. 展开更多
关键词 astrocyte CROSSTALK DEMYELINATION glial response microglia/macrophage multiple sclerosis neurodegeneration neuroinflammation oligodendrocyte lineage cells REMYELINATION
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电针上调Cezanne表达抑制NF-κB信号通路介导的大鼠脑缺血/再灌注炎性损伤 认领
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作者 卢文豪 周雪灵 +5 位作者 任义昆 王静文 朱君 胥虹贝 李佳妮 罗勇 《第三军医大学学报》 CAS 北大核心 2021年第4期283-294,共12页
目的探讨电针上调Cezanne的表达及对局灶脑缺血/再灌注大鼠炎性损伤的神经保护作用。方法将SD大鼠按简单随机分组分为假手术(sham)组、电针(EA)组、缺血/再灌注(MCAO/R)组和缺血/再灌注+电针(MCAO/R+EA)组,颅内注射Cezanne沉默慢病毒(LV... 目的探讨电针上调Cezanne的表达及对局灶脑缺血/再灌注大鼠炎性损伤的神经保护作用。方法将SD大鼠按简单随机分组分为假手术(sham)组、电针(EA)组、缺血/再灌注(MCAO/R)组和缺血/再灌注+电针(MCAO/R+EA)组,颅内注射Cezanne沉默慢病毒(LV-shCezanne),空载慢病毒(vehicle)作为对照。采用改良线栓法制备右侧大脑中动脉缺血/再灌注模型,电针刺激"百会"穴和病侧"四关"穴("合谷"/"太冲"穴)。缺血2 h后分别再灌注6、12、24、48、72 h和7 d。分别采用Garcia评分、TTC染色、Western blot、细胞计数,免疫荧光检测各组神经功能评分、梗死灶体积、缺血大脑皮质区Cezanne蛋白表达、Cezanne阳性细胞数、Cezanne的细胞分布类型、细胞核与细胞质NF-κB p65蛋白的表达。结果与sham组相比,EA组Cezanne蛋白表达在6 h和48 h增加(P<0.05),MCAO/R组Cezanne蛋白表达在12、24、48、72 h和7 d时增加(P<0.05);与MCAO/R组相比,MCAO/R+EA组Cezanne蛋白表达在12、24、72 h时进一步增加(P<0.05)。相较于sham组,MCAO/R组神经评分降低(P<0.05),Cezanne阳性细胞数、脑梗死体积增加(P<0.05);相较于MCAO/R组,MCAO/R+EA组神经评分升高(P<0.05),Cezanne阳性细胞数增多(P<0.05),脑梗死体积(P<0.05)、p-IκBα/IκBα比值(P<0.05)、细胞核p65/细胞质p65比值降低(P<0.05);免疫荧光显示Cezanne主要分布在缺血大脑皮质区神经元细胞质。结论电针通过上调Cezanne蛋白的表达,抑制大鼠局灶脑缺血/再灌注后NF-κB信号通路的激活,从而发挥神经保护作用。 展开更多
关键词 电针 锌指蛋白Cezanne 脑缺血/再灌注 神经炎症 NF-κB信号通路
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 被引量：1
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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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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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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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异丙酚介导的RhoA/ROCK2信号通路对脑缺血再灌注后神经炎症、细胞凋亡和脑梗死的作用 认领
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作者 鄢圣娟 王兆薇 +2 位作者 田亮 杨克俊 吴飞哥 《卒中与神经疾病》 2021年第1期14-19,共6页
目的探讨异丙酚对脑缺血再灌注大鼠神经炎症、细胞凋亡和脑梗死的作用与保护机制。方法将30只SD大鼠随机分为假手术(Sham)组、脑缺血再灌注(I/R)组和异丙酚(Propofol)组,Sham组与I/R组使用水合氯醛(300 mg/kg)麻醉,异丙酚组应用异丙酚(6... 目的探讨异丙酚对脑缺血再灌注大鼠神经炎症、细胞凋亡和脑梗死的作用与保护机制。方法将30只SD大鼠随机分为假手术(Sham)组、脑缺血再灌注(I/R)组和异丙酚(Propofol)组,Sham组与I/R组使用水合氯醛(300 mg/kg)麻醉,异丙酚组应用异丙酚(60mg/kg)麻醉;大脑中动脉闭塞造模2 h后恢复血供,24 h后进行神经功能缺损评分,取脑组织进行TTC染色、炎性细胞因子水平检测、免疫组化、Western blot实验。结果 I/R组大鼠神经功能受损,缺血侧梗死严重;Western Blot检测显示RhoA/ROCK2蛋白表达增加,Caspase-3蛋白剪切增加;免疫组化显示Iba1激活,GFAP活化,即神经炎症反应增加。此外,Nissl小体减少,TUNEL阳性细胞数增加,即神经元凋亡增加;异丙酚组RhoA/ROCK2蛋白表达水平、Caspase-3蛋白剪切显著降低,神经炎症反应减轻与神经元凋亡减少,神经功能缺损评分降低与脑梗死面积减少。结论异丙酚可能通过抑制RhoA/ROCK2信号通路来减轻脑中神经炎症反应和减少神经元凋亡,从而改善神经功能与脑部梗死情况。 展开更多
关键词 脑缺血再灌注 异丙酚 神经炎症 细胞凋亡 RhoA/ROCK2
神经炎症在动脉瘤性蛛网膜下腔出血后早期脑损伤中的作用 认领
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作者 廖艺斐 张慧 邹良玉 《中国卒中杂志》 2021年第1期92-96,共5页
早期脑损伤(early brain injury,EBI)是影响动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)患者预后的重要因素之一。目前aSAH后EBI产生机制尚不明确,神经炎症可能为其主要驱动因素,其作用机制包括:红细胞降解产物... 早期脑损伤(early brain injury,EBI)是影响动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)患者预后的重要因素之一。目前aSAH后EBI产生机制尚不明确,神经炎症可能为其主要驱动因素,其作用机制包括:红细胞降解产物和激活的小胶质细胞诱导神经炎症促进神经元凋亡;神经炎症通过激活星形胶质细胞破坏血脑屏障导致脑水肿,并募集外周中性粒细胞黏附于颅内微脉管系统引起微血管功能障碍导致脑皮质灌注不足。应用针对神经炎症不同靶点的药物预防EBI可能是当前治疗aSAH的新方向。 展开更多
关键词 动脉瘤性蛛网膜下腔出血 早期脑损伤 神经炎症
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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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小胶质细胞引起和促进阿尔茨海默病的研究进展 认领
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作者 王紫涵 罗金定 +2 位作者 田英入 奉水东 凌宏艳 《基础医学与临床》 2021年第2期277-281,共5页
小胶质细胞是神经系统免疫细胞,具有双重特性,既可以通过免疫反应增强吞噬能力、释放抗炎因子维持脑组织的稳态和保护神经元,又可以增加炎性反应、降低有害蛋白清除能力损伤神经元。受衰老的影响,在基因表达方面,小胶质细胞CD33表达增... 小胶质细胞是神经系统免疫细胞,具有双重特性,既可以通过免疫反应增强吞噬能力、释放抗炎因子维持脑组织的稳态和保护神经元,又可以增加炎性反应、降低有害蛋白清除能力损伤神经元。受衰老的影响,在基因表达方面,小胶质细胞CD33表达增加而髓系细胞触发受体2(TREM2)表达减少;在活化表型方面,衰老环境下的小胶质细胞更倾向活化为促炎表型,从而促进阿尔茨海默病(AD)的发生与进展。本文从小胶质细胞的基因表达、促炎表型和免疫调控3方面阐述小胶质细胞诱发和促进AD的途径及机制,以期通过小胶质细胞为AD治疗提供新的方向。 展开更多
关键词 阿尔茨海默病 小胶质细胞 神经炎性反应 免疫调控
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柚皮苷通过调节小胶质细胞极化对APPswe/PS1dE9双转基因小鼠的认知功能影响 认领
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作者 王贝 赵雨航 +3 位作者 王乐伟 潘顺基 石见 王冬梅 《中国比较医学杂志》 CAS 北大核心 2021年第2期1-7,共7页
目的探究柚皮苷(naringin)对APPswe/PS1dE9双转基因小鼠小胶质细胞极化的调节效应及该效应对Aβ聚集和认知功能的影响。方法3月龄APPswe/PS1dE9转基因雄性小鼠随机分为模型组(APPswe/PS1dE9)和柚皮苷治疗组(APPswe/PS1dE9+柚皮苷100 mg/... 目的探究柚皮苷(naringin)对APPswe/PS1dE9双转基因小鼠小胶质细胞极化的调节效应及该效应对Aβ聚集和认知功能的影响。方法3月龄APPswe/PS1dE9转基因雄性小鼠随机分为模型组(APPswe/PS1dE9)和柚皮苷治疗组(APPswe/PS1dE9+柚皮苷100 mg/(kg·d)),选择年龄体重匹配同窝非转基因小鼠作为阴性对照组和柚皮苷单独给药组(柚皮苷100 mg/(kg·d)),对照组及模型组给予常规的标准鼠粮,APPswe/PS1dE9+柚皮苷组和柚皮苷单独给药组在常规标准鼠粮中加入100 mg/(kg·d)的柚皮苷治疗16周。新物体识别实验检测小鼠非空间短期记忆能力;酶联免疫吸附法检测柚皮苷对小鼠肝肾功能的影响;q-PCR检测小鼠脑组织中小胶质细胞M1型和M2型标记物的表达;免疫荧光染色检测活化小胶质细胞对Aβ的吞噬作用以及Aβ的含量。结果与对照组相比,模型组小鼠新物体识别实验中识别指数显著降低(P<0.05),脑组织M1型标记物(CD16、TNF-α、i NOS、MCP-1)的mRNA表达水平均显著增加(P<0.05),而M2型标记物(CD206、TGF-β、Arg1、YM-1)的mRNA表达均显著降低(P<0.05),大脑皮层和海马的Aβ阳性区域明显增加(P<0.05)。与模型组相比,柚皮苷治疗组小鼠识别指数显著增加(P<0.05),M1型标记物mRNA表达水平均显著降低(P<0.05),M2型标记物mRNA表达均显著增加(P<0.05),促进小胶质细胞对Aβ的吞噬,Aβ免疫阳性区域显著减少(P<0.05)。各组之间小鼠肝肾功能各参数值无显著性差异(P>0.05)。结论柚皮苷通过调节小胶质细胞M1向M2的极化,进而促进活化的小胶质细胞对Aβ的吞噬,最终改善小鼠认知。 展开更多
关键词 柚皮苷 认知 小胶质细胞极化 神经炎症
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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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T细胞在阿尔兹海默氏病中的研究进展 认领
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作者 侯青松 霍燕 +1 位作者 方焕焕(综述) 段淑荣(审校) 《中风与神经疾病杂志》 CAS 2021年第2期178-181,共4页
阿尔茨海默氏病(Alzheimer'’s disease,AD)是一种与年龄相关性的慢性、进行性和不可逆性神经退行性疾病,其特征是认知和记忆障碍,是最为常见的痴呆类型。AD的病理学改变包括神经元外蛋白片段β-淀粉样蛋白(称为β-淀粉样蛋白,β-am... 阿尔茨海默氏病(Alzheimer'’s disease,AD)是一种与年龄相关性的慢性、进行性和不可逆性神经退行性疾病,其特征是认知和记忆障碍,是最为常见的痴呆类型。AD的病理学改变包括神经元外蛋白片段β-淀粉样蛋白(称为β-淀粉样蛋白,β-amyloid,Aβ)和神经元内蛋白tau蛋白(称为tau缠结)的异常形式的积累[1]。Aβ的积累会干扰突触中神经元与神经元的通讯,Tau缠结会阻止营养物质和其他必需分子在神经元内部的运输,导致细胞死亡。 展开更多
关键词 阿尔兹海默病 T细胞 神经炎症 细胞因子
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