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N-methyl-D-aspartate receptor subunit 1 regulates neurogenesis in the hippocampal dentate gyrus of schizophrenia-like mice 预览
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作者 Juan Ding Chun Zhang +4 位作者 Yi-Wei Zhang Quan-Rui Ma Yin-Ming Liu Tao Sun Juan Liu 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第12期2112-2117,共6页
N-methyl-D-aspartate receptor hypofunction is the basis of pathophysiology in schizophrenia. Blocking the N-methyl-D-aspartate receptor impairs learning and memory abilities and induces pathological changes in the bra... N-methyl-D-aspartate receptor hypofunction is the basis of pathophysiology in schizophrenia. Blocking the N-methyl-D-aspartate receptor impairs learning and memory abilities and induces pathological changes in the brain. Previous studies have paid little attention to the role of the N-methyl-D-aspartate receptor subunit 1 (NR1) in neurogenesis in the hippocampus of schizophrenia. A mouse model of schizophrenia was established by intraperitoneal injection of 0.6 mg/kg MK-801, once a day, for 14 days. In N-methyl-D-aspartate-treated mice, N-methyl-D-aspartate was administered by intracerebroventricular injection in schizophrenia mice on day 15. The number of NR1-, Ki67- or BrdU-immunoreactive cells in the dentate gyrus was measured by immunofluorescence staining. Our data showed the number of NR1-immunoreactive cells increased along with the decreasing numbers of BrdU- and Ki67-immunoreactive cells in the schizophrenia groups compared with the control group. N-methyl-D-aspartate could reverse the above changes. These results indicated that NR1 can regulate neurogenesis in the hippocampal dentate gyrus of schizophrenia mice, supporting NR1 as a promising therapeutic target in the treatment of schizophrenia. This study was approved by the Experimental Animal Ethics Committee of the Ningxia Medical University, China (approval No. 2014-014) on March 6, 2014. 展开更多
关键词 nerve REGENERATION SCHIZOPHRENIA MK-801 N-METHYL-D-ASPARTATE NEUROGENESIS N-METHYL-D-ASPARTATE receptor N-methyl-Daspartate receptor SUBUNIT 1 BrdU Ki67 HIPPOCAMPAL dentate gyrus HIPPOCAMPAL NEUROGENESIS neural REGENERATION
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停用丙戊酸对海马-空间工作记忆和神经发生损伤的改善作用
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作者 Wanassanun PANNANGRONG Apiwat SIRICHOAT +2 位作者 Trai WONGSIRI Peter WIGMORE Jariya Umka WELBAT 《浙江大学学报:B卷英文版》 SCIE CAS CSCD 2019年第3期253-263,共11页
目的:丙戊酸是一种用于治疗癫痫发作的药物,可引起成人和儿童的空间记忆障碍。海马的神经发生与学习能力密切相关,而丙戊酸可抑制该区域的神经发生,从而导致空间记忆障碍。我们已有动物模型证明丙戊酸能显著损害海马-空间工作记忆,并抑... 目的:丙戊酸是一种用于治疗癫痫发作的药物,可引起成人和儿童的空间记忆障碍。海马的神经发生与学习能力密切相关,而丙戊酸可抑制该区域的神经发生,从而导致空间记忆障碍。我们已有动物模型证明丙戊酸能显著损害海马-空间工作记忆,并抑制齿状回亚颗粒区域中的神经元生成。既往临床病例报道指出患者在停用丙戊酸治疗后记忆能力有所改善。因此,本实验研究停用丙戊酸治疗后两个时间点的空间记忆和海马神经发生的恢复情况。创新点:研究了停用丙戊酸后的空间记忆恢复的时间进程以及与海马神经发生变化之间的关系。方法:雄性Wistar大鼠每天两次腹膜内注射0.9%生理盐水或丙戊酸(300 mg/kg),持续10天。在药物治疗结束后第1、30或45天,使用新物体位置(NOL)测试来检查空间记忆;使用Ki67免疫组织化学计数海马细胞分裂情况;并使用免疫印迹法(western immunoblotting)测量脑源性神经营养因子(BDNF)和Notch1的水平。结论:药物治疗结束后第1天和第30天大鼠的空间工作记忆有受损,但在第45天时,恢复到正常水平。细胞增殖在第30天和第45天时增加至正常水平。神经发生的两种标志物(BDNF和Notch1)在第45天时恢复到正常水平。这些结果表明了记忆能力的恢复发生在停用丙戊酸6周内,并且该种效应发生在海马神经发生恢复至正常水平后。 展开更多
关键词 海马 神经发生 空间记忆 丙戊酸
m6A Regulates Neurogenesis and Neuronal Development by Modulating Histone Methyltransferase Ezh2
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作者 Junchen Chen Yi-Chang Zhang +8 位作者 Chunmin Huang Hui Shen Baofa Sun Xuejun Cheng Yu-Jie Zhang Yun-Gui Yang Qiang Shu Ying Yang Xuekun Li 《基因组蛋白质组与生物信息学报:英文版》 CAS CSCD 2019年第2期154-168,共15页
N6-methyladenosine (m6A),catalyzed by the methyltransferase complex consisting of Mettl3 and Mettl14,is the most abundant RNA modification in mRNAs and participates in diverse biological processes. However,the roles a... N6-methyladenosine (m6A),catalyzed by the methyltransferase complex consisting of Mettl3 and Mettl14,is the most abundant RNA modification in mRNAs and participates in diverse biological processes. However,the roles and precise mechanisms of m6A modification in regulating neuronal development and adult neurogenesis remain unclear. Here,we examined the function of Mettl3,the key component of the complex,in neuronal development and adult neurogenesis of mice. We found that the depletion of Mettl3 significantly reduced m6A levels in adult neural stem cells (aNSCs) and inhibited the proliferation of aNSCs. Mettl3 depletion not only inhibited neu-ronal development and skewed the differentiation of aNSCs more toward glial lineage,but also affected the morphological maturation of newborn neurons in the adult brain. m6A immunoprecip-itation combined with deep sequencing (MeRIP-seq) revealed that m6A was predominantly enriched in transcripts related to neurogenesis and neuronal development. Mechanistically,m6A was present on the transcripts of histone methyltransferase Ezh2,and its reduction upon Mettl3 knockdown decreased both Ezh2 protein expression and consequent H3K27me3 levels. The defects of neurogenesis and neuronal development induced by Mettl3 depletion could be rescued by Ezh2 overexpression. Collectively,our results uncover a crosstalk between RNA and histone modifica-tions and indicate that Mettl3-mediated m6A modification plays an important role in regulating neurogenesis and neuronal development through modulating Ezh2. 展开更多
关键词 N6-methyladenosine (m6A) Mettl3 NEUROGENESIS NEURONAL DEVELOPMENT EZH2
SSRI类药物对慢性应激神经发生的影响 预览
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作者 曹金明 王大力 +3 位作者 顾平 张君 孙耐 姜萌 《世界最新医学信息文摘(电子版)》 2019年第42期69-71,共3页
慢性应激与抑郁症的发病密切相关。通过调控HPA-Glu-NMDA受体-NO路径,慢性应激导致大脑尤其是海马结构的器质性损害,最终诱发抑郁症。神经发生持续存在于中枢神经系统,被认为是与慢性应激所致抑郁等脑损伤的修复具有密切关系,大量实验证... 慢性应激与抑郁症的发病密切相关。通过调控HPA-Glu-NMDA受体-NO路径,慢性应激导致大脑尤其是海马结构的器质性损害,最终诱发抑郁症。神经发生持续存在于中枢神经系统,被认为是与慢性应激所致抑郁等脑损伤的修复具有密切关系,大量实验证明,SSRI类药物对神经发生具有促进作用,海马、侧脑室等部位存在神经干细胞,能内源性激活神经发生,其可通过影响神经干细胞的增殖、定向分化、突触的再生及修复等促进伸进发生。本文就SSRI类药物对慢性应激神经发生的影响做一综述。 展开更多
关键词 选择性5-羟色胺再摄取抑制剂 慢性应激 神经发生 海马
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Leukemia Inhibitory Factor Decreases Neurogenesis and Angiogenesis in a Rat Model of Intracerebral Hemorrhage 预览
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作者 Chuan-zhen LIU Hua-jun ZHOU +5 位作者 Jian-hua ZHONG Tao TANG Han-jin CUI Jing-hua ZHOU Qiang ZHANG Zhi-gang MEI 《当代医学科学(英文)》 SCIE CAS 2019年第2期298-304,共7页
Neurogenesis and angiogenesis can improve the neurologic function after intracerebral hemorrhage(ICH).Leukemia inhibitory factor(LIF)plays an important role in neurogenesis and angiogenesis.In this study,a rat model o... Neurogenesis and angiogenesis can improve the neurologic function after intracerebral hemorrhage(ICH).Leukemia inhibitory factor(LIF)plays an important role in neurogenesis and angiogenesis.In this study,a rat model of autologous blood-induced ICH was used to evaluate the effect of LIF on the neurogenesis and angiogenesis following ICH.After ICH,LIF-positive neurons and dilated vessels were detected in the peri-hematomal region.It was found that LIF levels increased significantly and peaked 14 days after ICH induction.Double immunofluorescence confirmed that LIF was expressed in neurons and endothelial cells.ICH also led to increases of doublecortin(DCX)-and von Willebrand factor(vWF)-positive cells as well as proliferation of cell nuclear antigen(PCNA)+/DCX+and PCNA+/vWF+nuclei.All these ICH-induced increases were significantly attenuated by exogenous LIF in fusion.These data suggested that LIF was a negative regulator of neurogenesis and angiogenesis after ICH. 展开更多
关键词 INTRACEREBRAL hemorrhage NEUROGENESIS ANGIOGENESIS LEUKEMIA INHIBITORY factor
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P2X7 receptor signaling during adult hippocampal neurogenesis 预览
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作者 Hannah C. Leeson Tailoi Chan-Ling +3 位作者 Michael D. Lovelace Jeremy C. Brownlie Ben J. Gu Michael W. Weible II 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1684-1694,共11页
Neurogenesis is a persistent and essential feature of the adult mammalian hippocampus.Granular neurons generated from resident pools of stem or progenitor cells provide a mechanism for the formation and consolidation ... Neurogenesis is a persistent and essential feature of the adult mammalian hippocampus.Granular neurons generated from resident pools of stem or progenitor cells provide a mechanism for the formation and consolidation of new memories.Regulation of hippocampal neurogenesis is complex and multifaceted,and numerous signaling pathways converge to modulate cell proliferation,apoptosis,and clearance of cellular debris,as well as synaptic integration of newborn immature neurons.The expression of functional P2X7 receptors in the central nervous system has attracted much interest and the regulatory role of this purinergic receptor during adult neurogenesis has only recently begun to be explored.P2X7 receptors are exceptionally versatile:in their canonical role they act as adenosine triphosphate-gated calcium channels and facilitate calcium-signaling cascades exerting control over the cell via calcium-encoded sensory proteins and transcription factor activation.P2X7 also mediates transmembrane pore formation to regulate cytokine release and facilitate extracellular communication,and when persistently stimulated by high extracellular adenosine triphosphate levels large P2X7 pores form,which induce apoptotic cell death through cytosolic ion dysregulation.Lastly,as a scavenger receptor P2X7 directly facilitates phagocytosis of the cellular debris that arises during neurogenesis,as well as during some disease states.Understanding how P2X7 receptors regulate the physiology of stem and progenitor cells in the adult hippocampus is an important step towards developing useful therapeutic models for regenerative medicine.This review considers the relevant aspects of adult hippocampal neurogenesis and explores how P2X7 receptor activity may influence the molecular physiology of the hippocampus,and neural stem and progenitor cells. 展开更多
关键词 P2X7 P2X7R adult NEUROGENESIS NEURAL stem CELLS NEURAL PROGENITOR CELLS hippocampus SGZ calcium SIGNALING PURINERGIC SIGNALING
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Neurogenesis in the hippocampus of adult humans: controversy "fixed" at last 预览
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作者 Silene M.A. Lima Walace Gomes-Leal 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期1917-1918,共2页
The presence of adult neurogenesis in the mammalian brain has been a theme of intense controversy for a long time since the original report by Altman and Das (1965). The scientific community, for about 30 years, has d... The presence of adult neurogenesis in the mammalian brain has been a theme of intense controversy for a long time since the original report by Altman and Das (1965). The scientific community, for about 30 years, has difficulties to accept that progenitor cells give rise to new neurons in some specific regions of the mammalian adult brain, the neurogenic niches (Kuhn et al., 1996;Doetsch et al., 1997, 1999). 展开更多
关键词 NEUROGENESIS HIPPOCAMPUS MAMMALIAN BRAIN
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运动上调蛋白酶体活性促进SVZ区神经发生
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作者 黄菲菲 王必慧 +2 位作者 赵泳媚 冯英楠 陆利 《中国运动医学杂志》 CAS CSCD 北大核心 2019年第2期126-130,共5页
目的:观察运动后小鼠脑室室管膜下区(subventricular zone,SVZ)蛋白酶体活性变化,探讨运动促进神经发生的机制。方法:应用荧光分光光度法检测新生小鼠(Postnantal day 0,P0)、成年小鼠(Postnantal day 90,P90)及老年小鼠(Postnantal day... 目的:观察运动后小鼠脑室室管膜下区(subventricular zone,SVZ)蛋白酶体活性变化,探讨运动促进神经发生的机制。方法:应用荧光分光光度法检测新生小鼠(Postnantal day 0,P0)、成年小鼠(Postnantal day 90,P90)及老年小鼠(Postnantal day 540,P540)SVZ蛋白酶体活性。成年小鼠自主跑轮运动4周后检测蛋白酶体活性,通过Ki67、DCX免疫荧光染色检测SVZ神经发生水平;小鼠注射MG132,观察抑制蛋白酶体活性是否影响运动对神经发生的促进作用。结果:随年龄增长,P90、P540小鼠SVZ蛋白酶体活性较P0小鼠分别下降50.9%(P<0.01)、70.4%(P<0.01)。运动后小鼠SVZ蛋白酶体活性较安静组增加39.8%(P<0.01),蛋白酶体亚单位PSMB1、PSMB2、PSMB5及PSMA3的表达水平也较安静组分别增加9.1%(P<0.05)、21.7%(P<0.01)、25.4%(P<0.01)和10.1%(P<0.05),神经发生相关指标Ki67^+、DCX^+细胞数量较安静组分别增加32.4%(P<0.01)和78.3%(P<0.001)。小鼠侧脑室注射MG132后再进行跑轮运动,MG132-运动组SVZ区Ki67^+、DCX^+细胞数量较DMSO-运动组分别下降27.6%(P<0.001)和51.5%(P<0.001)。结论:随年龄增长,蛋白酶体活性下降。运动可能通过提高SVZ蛋白酶体活性促进神经发生。 展开更多
关键词 衰老 蛋白酶体 运动 MG132 神经发生
Melatonin modifies SOX2~+ cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation 预览
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作者 Alan Hinojosa-Godínez Luis F. Jave-Suarez +5 位作者 Mario Flores-Soto Alma Y. Gálvez-Contreras Sonia Luquín Edith Oregon-Romero Oscar González-Pérez Rocio E. González-Castaneda 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1787-1795,共9页
Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep depri... Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep deprivation.The precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this process.In this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword clusterization.Our results showed that the administration of melatonin under sleep-deprived conditions increased the MECP2 expression and reduced the SIRT1 expression in the dentate gyrus.We observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep deprivation.In addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated group.These findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived conditions.All procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval No.CI-16610)on January 2,2016. 展开更多
关键词 sleep-deprivation MELATONIN microRNA NEUROGENESIS SIRTUIN 1 SIRT1 methyl-CpG-binding protein 2 MECP2 epigenetic text-mining mir-9 let-7b
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Sodium butyrate prevents radiation-induced cognitive impairment by restoring pCREB/BDNF expression 预览
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作者 Hae June Lee Yeonghoon Son +6 位作者 Minyoung Lee Changjong Moon Sung Ho Kim In Sik Shin Miyoung Yang Sangwoo Bae Joong Sun Kim 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第9期1530-1535,共6页
Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages.To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in anim... Sodium butyrate is a histone deacetylase inhibitor that affects various types of brain damages.To investigate the effects of sodium butyrate on hippocampal dysfunction that occurs after whole-brain irradiation in animal models and the effect of sodium butyrate on radiation exposure-induced cognitive impairments,adult C57BL/6 mice were intraperitoneally treated with 0.6 g/kg sodium butyrate before exposure to 10 Gy cranial irradiation.Cognitive impairment in adult C57BL/6 mice was evaluated via an object recognition test 30 days after irradiation.We also detected the expression levels of neurogenic cell markers(doublecortin)and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor.Radiation-exposed mice had decreased cognitive function and hippocampal doublecortin and phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression.Sodium butyrate pretreatment reversed these changes.These findings suggest that sodium butyrate can improve radiation-induced cognitive dysfunction through inhibiting the decrease in hippocampal phosphorylated cAMP response element binding protein/brain-derived neurotrophic factor expression.The study procedures were approved by the Institutional Animal Care and Use Committee of Korea Institute of Radiological Medical Sciences(approval No.KIRAMS16-0002)on December 30,2016. 展开更多
关键词 sodium BUTYRATE RADIOPROTECTOR ionizing radiation hippocampal damage cAMP response element binding BRAIN-DERIVED NEUROTROPHIC factor histone DEACETYLASE inhibitor neurogenesis
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Physiological and pathological effects of amyloid-β species in neural stem cell biology 预览
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作者 Adela Bernabeu-Zornoza Raquel Coronel +3 位作者 Charlotte Palmer María Monteagudo Alberto Zambrano Isabel Liste 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第12期2035-2042,共8页
Although amyloid-β peptide is considered neurotoxic, it may mediate several physiological processes during embryonic development and in the adult brain. The pathological function of amyloid-β peptide has been extens... Although amyloid-β peptide is considered neurotoxic, it may mediate several physiological processes during embryonic development and in the adult brain. The pathological function of amyloid-β peptide has been extensively studied due to its implication in Alzheimer’s disease, but its physiological function remains poorly understood. Amyloid-β peptide can be detected in non-aggregated (monomeric) and aggregated (oligomeric and fibrillary) forms. Each form has different cytotoxic and/or physiological properties, so amyloid-β peptide and its role in Alzheimer’s disease need to be studied further. Neural stem cells and neural precursor cells are good tools for the study on neurodegenerative diseases and can provide future therapeutic applications in diseases such as Alzheimer’s disease. In this review, we provide an outline of the effects of amyloid-β peptide, in monomeric and aggregated forms, on the biology of neural stem cells/neural precursor cells, and discuss the controversies. We also describe the possible molecular targets that could be implicated in these effects, especially GSK3β. A better understanding of amyloid-β peptide (both physiological and pathological), and the signaling pathways involved are essential to advance the field of Alzheimer’s disease. 展开更多
关键词 amyloid-β peptide NEURAL stem CELLS NEURAL PROGENITOR CELLS Alzheimer's disease AMYLOID precursor protein toxicity NEUROGENESIS gliogenesis GSK3β
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人脐静脉内皮细胞来源外泌体有助于促进缺血性脑卒中小鼠的康复 预览
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作者 张晓星 胡慧 李跃华 《中国临床医学》 2019年第3期425-431,共7页
目的:探讨人脐静脉内皮细胞(HUVECs)来源的外泌体对缺血性脑卒中小鼠的治疗效果。方法:提取并鉴定HUVECs细胞来源的外泌体(HUVECs-exo),尾静脉注射30μg(溶于100μLPBS中)外泌体至短暂性大脑中动脉缺血性模型小鼠体内,对照组注射同等体... 目的:探讨人脐静脉内皮细胞(HUVECs)来源的外泌体对缺血性脑卒中小鼠的治疗效果。方法:提取并鉴定HUVECs细胞来源的外泌体(HUVECs-exo),尾静脉注射30μg(溶于100μLPBS中)外泌体至短暂性大脑中动脉缺血性模型小鼠体内,对照组注射同等体积的PBS。术后第1、3、7、14、21、28天对小鼠进行mNSS评分,磁共振成像检测小鼠的梗死范围,在第28天将小鼠断头取脑,CD31/BrdU、DCX/BrdU、NeuN/BrdU免疫荧光双染评价小鼠梗死边缘区血管及神经元的新生,Western印迹法检测小鼠梗死边缘区突触前膜蛋白Synaptophysin及突触后膜蛋白PSD-95的表达情况,进而检测突触重塑。结果:HUVECs-exo组小鼠梗死范围显著小于PBS对照组(P<0.05),梗死边缘区新生血管、神经前体细胞及成熟神经元显著高于PBS对照组(P<0.05),HUVECs-exo组突触前膜蛋白Synaptophysin及后膜蛋白PSD-95表达含量显著高于PBS对照组(P<0.05)。HUVECs-exo组及PBS对照组在造模后第1、3、7天,神经功能评分无明显差异,在第14、21、28天HUVECs-exo组神经功能评分显著低于PBS对照组(P<0.05)。结论:HUVECs-exo尾静脉注射能够减小缺血性脑卒中后的梗死范围,促进梗死边缘区血管及神经元新生,促进突触重塑,改善卒中后的神经功能预后。 展开更多
关键词 缺血性脑卒中 外泌体 神经新生 血管新生 突触重塑
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褪黑素对慢性脑低灌注大鼠海马齿状回区神经再生的影响
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作者 王少朋 王茹 +4 位作者 李丹丹 马芮 赵弘轶 黄勇华 迟丽屹 《现代生物医学进展》 CAS 2019年第7期1251-1256,1265共7页
目的:研究褪黑素在慢性脑低灌注(Chronic Cerebral Hypoperfusion,CCH)大鼠模型中对神经再生的作用及机制。方法:使用双侧颈总动脉结扎法(bilateral common carotid artery occlusion,BCCAO)制备大鼠CCH模型,80只雄性的SD大鼠随机分为4... 目的:研究褪黑素在慢性脑低灌注(Chronic Cerebral Hypoperfusion,CCH)大鼠模型中对神经再生的作用及机制。方法:使用双侧颈总动脉结扎法(bilateral common carotid artery occlusion,BCCAO)制备大鼠CCH模型,80只雄性的SD大鼠随机分为4组,每组20只:生理盐水治疗假手术组(Sham组)、生理盐水治疗模型组(BCCAO组)、褪黑素(5 mg/kg)治疗模型组(MT1组)、褪黑素(10 mg/kg)治疗模型组(MT2组)。连续腹腔注射褪黑素或生理盐水共4周。利用挖掘实验评估大鼠行为学;使用HE染色观察神经细胞变性及坏死;采取尼氏染色法观察大鼠海马齿状回区神经元损伤情况;利用免疫荧光法测定神经元特异核蛋白(NeuN)、胶质纤维酸性蛋白(Ki67)、双皮质素(DCX)的表达;利用Western Blot法测定大鼠海马区脑源性神经营养因子(BDNF)、酪氨酸激酶B受体(TrkB)含量的表达。结果:和Sham组相比,BCCAO组大鼠挖掘能力明显下降(P<0.01),HE和尼氏染色出现神经细胞大量坏死、数量减少,NeuN阳性细胞数增加(P<0.01)、Ki67/DCX阳性细胞数无明显增加(P>0.05),BDNF、TrkB蛋白含量明显低于假手术组(P<0.01)。与BCCAO组相比,MT1组和MT2组大鼠挖掘能力均明显改善(P<0.01),HE和尼氏染色显示神经元存活数量增加,MT1组NeuN阳性细胞数增加(P<0.05)、Ki67/DCX阳性细胞数增加(P<0.05),MT2组NeuN、Ki67/DCX阳性细胞数明显增加(P<0.01),MT1组及MT2组BDNF、TrkB蛋白含量明显增加(P<0.01)。结论:褪黑素促进了CCH大鼠海马齿状回区神经再生和行为学的改变,其机制可能与激活BDNF-TrkB信号转导通路有关。 展开更多
关键词 褪黑素 海马 脑低灌注 神经再生
小分子混合物在神经诱导液中对根尖牙乳头干细胞成神经分化的影响 预览
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作者 陈琪欣 袁长永 +3 位作者 刘宗响 朱绍跃 胡刚刚 王鹏来 《中华口腔医学研究杂志(电子版)》 CAS 2019年第2期71-76,共6页
目的评估小分子混合物在神经诱导液中对根尖牙乳头干细胞(SCAP)向神经细胞分化能力的影响。方法分别使用神经诱导液(对照组)和添加小分子混合物的神经诱导液(实验组)培养SCAP,8d后在倒置显微镜下进行形态学观察,使用实时荧光定量聚合酶... 目的评估小分子混合物在神经诱导液中对根尖牙乳头干细胞(SCAP)向神经细胞分化能力的影响。方法分别使用神经诱导液(对照组)和添加小分子混合物的神经诱导液(实验组)培养SCAP,8d后在倒置显微镜下进行形态学观察,使用实时荧光定量聚合酶链反应(PCR)和免疫蛋白印迹法检测神经丝(NFM)、微管相关蛋白2(MAP2)和神经元特异性烯醇化酶(NSE)的表达情况,使用免疫荧光反应实验检测β3微管蛋白(TUBB3)的表达情况。采用SPSS16.0软件包对数据进行统计学分析。结果形态学观察结果显示,实验组SCAP形成了更多神经样突触。实时荧光定量PCR结果显示,实验组NFM、MAP2和NSE的mRNA相对表达量分别为6.608±2.836、29.40±6.645和6.428±1.025,较对照组(1.074±0.202、1.092±0.115和1.140±0.281)显著提高,差异均有统计学意义(tNFM=3.387,PNFM=0.0276;tMAP2=7.490,PMAP2=0.0017;tNSE=8.615,PNSE=0.0010)。免疫蛋白印迹实验结果显示,实验组NFM、MAP2和NSE印迹较对照组更为明显。免疫荧光反应实验结果显示,实验组SCAP中TUBB3表达明显强于对照组。结论小分子混合物添加入神经诱导液中能够促进SCAP向神经细胞分化。 展开更多
关键词 干细胞 牙乳头 神经发生 小分子混合物 神经诱导液
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The detrimental effects of lipopolysaccharideinduced neuroinflammation on adult hippocampal neurogenesis depend on the duration of the pro-inflammatory response 预览
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作者 Martha Pérez-Domínguez Evangelina Aila-Munz +1 位作者 Eduardo Domínguez-Rivas Angélica Zepeda 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第5期817-825,共9页
Adult hippocampal neurogenesis is a finely tuned process regulated by extrinsic factors.Neuroinflammation is a hallmark of several pathological conditions underlying dysregulation of neurogenesis.In animal models,lipo... Adult hippocampal neurogenesis is a finely tuned process regulated by extrinsic factors.Neuroinflammation is a hallmark of several pathological conditions underlying dysregulation of neurogenesis.In animal models,lipopolysaccharide(LPS)-induced neuroinflammation leads to a neurogenic decrease mainly associated to the early inflammatory response.However,it is not well understood how the neuroinflammatory response progresses over time and if neurogenesis continues to be diminished during the late neuroinflammatory response.Moreover,it is unknown if repeated intermittent administration of LPS along time induces a greater reduction in neurogenesis.We administered one single intraperitoneal injection of LPS or saline or four repeated injections(one per week)of LPS or saline to young-adult mice.A cohort of new cells was labeled with three 5-bromo-2-deoxyuridine injections(one per day)4 days after the last LPS injection.We evaluated systemic and neuroinflammation-associated parameters and compared the effects of the late neuroinflammatory response on neurogenesis induced by each protocol.Our results show that 1)a single LPS injection leads to a late pro-inflammatory response characterized by microglial activation,moderate astrocytic reaction and increased interleukin-6 levels.This response correlates in time with decreased neurogenesis and 2)a repeated intermittent injection of LPS does not elicit a late pro-inflammatory response although activated microglia persists.The latter profile is not accompanied by a continued longterm hippocampal neurogenic decrease.Hereby,we provide evidence that the neuroinflammatory response is a dynamic process that progresses in a milieu-dependent manner and does not necessarily lead to a neurogenic decrease,highlighting the complex interaction between the immune system and neurogenesis. 展开更多
关键词 DENTATE GYRUS subgranular zone inflammation microglia ASTROCYTES IL-6 cytokines cell proliferation neural progenitor cells IMMATURE neurons long-term short-term adult hippocampal NEUROGENESIS
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金钱鱼Dmrt5基因的克隆及表达分析 预览
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作者 古皓天 刘倩晴 +4 位作者 司徒家欣 江东能 陈华谱 吴天利 李广丽 《海南热带海洋学院学报》 2019年第2期9-15,共7页
为了解金钱鱼Dmrt5在性腺中的作用,克隆了金钱鱼Dmrt5,采用逆转录PCR检测了它的组织分布,并采用荧光定量PCR检测了Dmrt5在性腺和胚胎期中的表达模式.实验结果表明,金钱鱼Dmrt5的ORF全长为1347bp,编码蛋白含448个氨基酸残基.同源性分析发... 为了解金钱鱼Dmrt5在性腺中的作用,克隆了金钱鱼Dmrt5,采用逆转录PCR检测了它的组织分布,并采用荧光定量PCR检测了Dmrt5在性腺和胚胎期中的表达模式.实验结果表明,金钱鱼Dmrt5的ORF全长为1347bp,编码蛋白含448个氨基酸残基.同源性分析发现,金钱鱼Dmrt5与橙线雀的相似性最高为96.0%,与人的相似性最低为68.0%.通过系统进化分析可知金钱鱼Dmrt5与鲈形目鱼类Dmrt5为一类,与其进化地位一致.组织分布表明,金钱鱼Dmrt5在下丘脑和脑垂体中高表达.对性腺不同发育时期的表达分析发现,Dmrt5在Ⅲ期和Ⅳ期精巢中的表达显著高于Ⅴ期精巢,而在Ⅱ、Ⅲ、Ⅳ期卵巢间的表达无显著差异.Dmrt5在胚胎期各阶段都有表达,但差异不显著.金钱鱼Dmrt5可能具有性别调控和神经发生等功能. 展开更多
关键词 金钱鱼 Dmrt5 克隆 组织表达 性腺 胚胎期 神经发生
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Akt/mTOR信号通路在氨甲酰促红细胞生成素促进脑梗死后神经发生作用的研究 预览
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作者 李洋 闫保君 《中风与神经疾病杂志》 CAS 2019年第6期509-512,共4页
目的探讨Akt/mTOR信号通路在氨甲酰促红细胞生成素(carbamylated erythropoietin,CEPO)促进脑梗死后室管膜下区(subventricular zone,SVZ)神经发生的作用。方法按随机数字表法将雄性小鼠分为Sham组、MCAO组、CEPO组和GSK2141795(Akt阻断... 目的探讨Akt/mTOR信号通路在氨甲酰促红细胞生成素(carbamylated erythropoietin,CEPO)促进脑梗死后室管膜下区(subventricular zone,SVZ)神经发生的作用。方法按随机数字表法将雄性小鼠分为Sham组、MCAO组、CEPO组和GSK2141795(Akt阻断剂)组。运用线栓法制作小鼠大脑中动脉闭塞模型。用改良的神经功能评分评价神经功能恢复状况。用5-溴-2-脱氧尿嘧啶核苷(5-bromo-2-deoxyuridine,BrdU)标记增殖细胞,巢蛋白(Nestin)标记神经干细胞,应用免疫荧光技术观察各组小鼠SVZ中BrdU^+/Nestin^+细胞的表达情况,Western blot技术测定各组小鼠SVZ内p-Akt和p-mTOR蛋白表达量的变化情况。结果GSK组小鼠在各评估时间点神经功能评分分值较CEPO组显著提高,差异有统计学意义(P<0.05)。术后7 d,GSK组小鼠SVZ中BrdU^+/Nestin^+细胞数,p-Akt和p-mTOR蛋白表达量较CEPO组显著减少(P<0.05)。结论CEPO可促进脑梗死后SVZ内神经干细胞增殖,这一过程可能是通过Akt/mTOR信号通路完成的。 展开更多
关键词 氨甲酰促红细胞生成素 Akt/mTOR信号通路 室管膜下区 脑卒中 神经发生
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Aging gracefully: social engagement joins exercise and enrichment as a key lifestyle factor in resistance to age-related cognitive decline 预览
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作者 Tyler J. Dause Elizabeth D. Kirby 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第1期39-42,共4页
关键词 生活方式 年龄相关 社会 衰落 啮齿类动物 优雅 老化过程 动物模型
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Wnt/β-catenin信号介导的小鼠海马神经元发生参与睡眠剥夺引起的学习记忆下降
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作者 屈杜洁 郇宇 +4 位作者 赵又谊 黄鑫 霍芳芳 王亚周 吴中亮 《神经解剖学杂志》 CAS CSCD 北大核心 2019年第2期134-140,共7页
目的:研究睡眠剥夺对小鼠行为及海马神经元发生的影响。从Wnt/β-catenin信号的角度探索其相关的分子机制,以及干预Wnt/β-catenin信号的改善作用。方法:采用改良多平台水环境法制作小鼠睡眠剥夺模型(SD)。利用Brd U/DCX免疫荧光双标研... 目的:研究睡眠剥夺对小鼠行为及海马神经元发生的影响。从Wnt/β-catenin信号的角度探索其相关的分子机制,以及干预Wnt/β-catenin信号的改善作用。方法:采用改良多平台水环境法制作小鼠睡眠剥夺模型(SD)。利用Brd U/DCX免疫荧光双标研究海马神经元发生;采用Wnt信号报告基因Topgal小鼠研究Wnt信号的改变;利用Nestin/ROSA/EX3基因修饰小鼠研究激活Wnt信号对睡眠剥夺小鼠海马神经元发生及学习记忆的影响;采用高架十字迷宫和旷场实验评估小鼠的焦虑情绪;运用Morris水迷宫评估小鼠的空间学习记忆能力。结果:与正常小鼠相比,SD处理组小鼠无焦虑样行为,但空间学习记忆能力显著下降。Brd U/DCX免疫荧光双标染色显示SD 5 d后小鼠海马神经元发生明显减弱。Wnt信号报告基因β-gal在海马神经干细胞表达降低。在Nestin/ROSA/EX3基因修饰小鼠激活Wnt信号后,可显著促进海马神经元发生,并改善SD小鼠的空间记忆能力。结论:Wnt/β-catenin信号参与睡眠剥夺引起的小鼠海马神经元发生减弱,增强Wnt信号可改善SD小鼠海马的神经元发生及其学习记忆能力。 展开更多
关键词 睡眠剥夺 海马 神经元发生 Wnt/β-catenin信号 学习记忆 小鼠
Active Compounds and Molecular Targets of Chinese Herbal Medicine for Neurogenesis in Stroke Treatment: Implication for Cross Talk between Traditional Chinese Medicine and Biomedical Sciences
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作者 Xi Chen Han-Sen Chen +1 位作者 Cheng Peng Jian-Gang Shen 《世界中医药杂志:英文版》 2019年第2期104-115,共12页
Neural stem/progenitor cells (NSCs) could be attractive therapeutic targets for promoting adult neurogenesis, brain plasticity, and repair in stroke and neurodegenerative diseases, raising great potentials for regener... Neural stem/progenitor cells (NSCs) could be attractive therapeutic targets for promoting adult neurogenesis, brain plasticity, and repair in stroke and neurodegenerative diseases, raising great potentials for regeneration therapy. In adult ischemic brains, NSCs have limited capacities of growth, differentiation, and generating new neurons for repairing the damaged central nervous system. However, the spontaneous brain repair seems to be insufficient to recover neurological deficits in most stroke cases. To overcome those problems, pharmacological manipulations targeting on endogenous NSCs or transplanted stem cells could be a promoting strategy for regeneration therapy. Chinese herbal medicine has great potentials for developing novel therapeutic strategies for adult neurogenesis and brain repair in poststroke treatment. Chinese herbal medicine has a long history for poststroke treatment. Recent studies create great opportunity for drug discovery for promoting neurogenesis and improving the recovery of neurological fimctions in poststroke treatment. Many active compounds or extracts from medicinal herbs have shown promising effects on regulating proliferation, self-renewal and differentiation of NSCs, and promoting neural network formation as well as neurological functional recovery with in vitro and in vivo experimental evidence. Therefore, targeting neural stem/progenitor cells can be an important opportunity for the studies of Traditional Chinese Medicine in regeneration medicine. Due to the complex interactions of herbal ingredients in network regulation, huge challenge remains to be resolved for further study. 展开更多
关键词 Chinese HERBAL medicine NEUROGENESIS STROKE
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