|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Mesenchymal stem cells and the neuronal microenvironment in the area of spinal cord injury显示文摘Cell-based technologies are used as a therapeutic strategy in spinal cord injury(SCI). Mesenchymal stem cells(MSCs), which secrete various neurotrophic factors and cytokines, have immunomodulatory, anti-apoptotic and anti-inflammatory effects, modulate reactivity/phenotype of astrocytes and the microglia, thereby promoting neuroregeneration seem to be the most promising. The therapeutic effect of MSCs is due to a paracrine mechanism of their action, therefore the survival of MSCs and their secretory phenotype is of particular importance. Nevertheless, these data are not always reported in efficacy studies of MSC therapy in SCI. Here, we provide a review with summaries of preclinical trials data evaluating the efficacy of MSCs in animal models of SCI. Based on the data collected, we have tried(1) to establish the behavior of MSCs after transplantation in SCI with an evaluation of cell survival, migration potential, distribution in the area of injured and intact tissue and possible differentiation;(2) to determine the effects MSCs on neuronal microenvironment and correlate them with the efficacy of functional recovery in SCI;(3) to ascertain the conditions under which MSCs demonstrate their best survival and greatest efficacy. | Yana O.Mukhamedshina Olga A.Gracheva Dina M.Mukhutdinova Yurii A.Chelyshev Albert A.Rizvanov | 2019 | Neural Regeneration Research2019，14，2： | 25 |
| 2 | Low-dose metformin treatment in the subacute phase improves the locomotor function of a mouse model of spinal cord injury显示文摘Metformin,a first-line drug for type-2 diabetes,has been shown to improve locomotor recovery after spinal cord injury.However,there are studies reporting no beneficial effect.Recently,we found that high dose of metformin(200 mg/kg,intraperitoneal)and acute phase administration(immediately after injury)led to increased mortality and limited locomotor function recovery.Consequently,we used a lower dose(100 mg/kg,i.p.)metformin in mice,and compared the effect of immediate administration after spinal cord injury(acute phase)with that of administration at 3 days post-injury(subacute phase).Our data showed that metformin treatment starting at the subacute phase significantly improved mouse locomotor function evaluated by Basso Mouse Scale(BMS)scoring.Immunohistochemical studies also revealed significant inhibitions of microglia/macrophage activation and astrogliosis at the lesion site.Furthermore,metformin treatment at the subacute phase reduced neutrophil infiltration.These changes were in parallel with the increased survival rate of spinal neurons in animals treated with metformin.These findings suggest that low-dose metformin treatment for subacute spinal cord injury can effectively improve the functional recovery possibly through anti-inflammation and neuroprotection.This study was approved by the Institute Animal Care and Use Committee at the University of Texas Medical Branch(approval No.1008041C)in 2010. | Wen-Ye Song Han Ding Tiffany Dunn Jun-Ling Gao Javier Allende Labastida Caitlin Schlagal Guang-Zhi Ning Shi-Qing Feng Ping Wu | 2021 | Neural Regeneration Research2021，16，11： | 12 |
| 3 | Current status of cell-mediated regenerative therapies for human spinal cord injury显示文摘During the past decade, significant advances have been made in refinements for regenerative therapies following human spinal cord injury(SCI).Positive results have been achieved with different types of cells in various clinical studies of SCI.In this review, we summarize recently-completed clinical trials using cellmediated regenerative therapies for human SCI, together with ongoing trials using neural stem cells.Specifically, clinical studies published in Chinese journals are included.These studies show that current transplantation therapies are relatively safe, and have provided varying degrees of neurological recovery.However, many obstacles exist, hindering the introduction of a specifi c clinical therapy, including complications and their causes, selection of the target population, and optimization of transplantation material.Despite these and other challenges, with the collaboration of research groups and strong support from various organizations, cell-mediated regenerative therapies will open new perspectives for SCI treatment. | Tongming Zhu Qisheng Tang Huasong Gao Yiwen Shen Luping Chen Jianhong Zhu | 2014 | Neuroscience Bulletin2014，30，4： | 7 |
| 4 | 间充质干细胞对脊髓损伤治疗的研究进展显示文摘背景:脊髓损伤是人类致残率最高的疾病之一,由于脊髓轴突再生能力有限,恢复难度大,常导致严重的神经后遗症,对脊髓损伤治疗方法的探索已成为研究热点。随着生物学及分子生物学研究的不断深入,研究发现间充质干细胞治疗脊髓损伤表现出巨大的潜力,为脊髓损伤的修复带来了曙光。目的:综述间充质干细胞对于脊髓损伤的治疗作用、性质、应用、局限性及发展前景。方法:检索PubMed、Web of Science数据库及万方、CNKI中国期刊全文数据库收录的间充质干细胞治疗脊髓损伤的相关文章,英文检索词为“spinal cord injury,mesenchymal stem cell”,中文检索词为“脊髓损伤,间充质干细胞”,按纳入和排除标准共纳入文献85篇进行归纳总结。结果与结论:间充质干细胞通过多种作用机制修复脊髓损伤,如间充质干细胞体内移植后通过分化为神经细胞替代已损伤的神经元;通过旁分泌机制分泌各种营养物质来改变脊髓损伤微环境的变化;同时间充质干细胞产生多种细胞外基质,为再生轴突提供支持物,促进神经元轴突再生。虽然在基础实验中间充质干细胞治疗脊髓损伤能起到较好的疗效,但间充质干细胞在临床中的应用却差强人意,还需要更深入地探索间充质干细胞对于脊髓损伤的作用机制。 | 史旭 刘京松 万然 王岩松 | 2020 | 中国组织工程研究2020，24，25： | 7 |
| 5 | 星形胶质细胞作为脊髓损伤治疗靶细胞的研究进展显示文摘脊髓损伤(spinal cord injury,SCI)往往导致严重的感觉和运动神经功能障碍,目前尚无理想的治疗方法。因此,需要进一步深入研究SCI修复的病理机制,探索有效的治疗策略,特别是寻找有效的治疗靶细胞。星形胶质细胞是中枢神经系统(central nervous system,CNS)的一类胶质细胞,在正常和损伤的CNS中均扮演了重要而复杂的角色,已成为神经科学家关注的焦点。近年来的研究表明,星形胶质细胞是SCI治疗的一个理想靶细胞。本文就星形胶质细胞在SCI病理反应中的作用、星形胶质细胞移植以及星形胶质细胞重编程等方面的研究进展作一综述。 | 黄潇 谷亚坤 程雪燕 苏志达 | 2017 | 生理学报2017，69，6： | 7 |
| 6 | 拓扑异构酶Ⅱ的结构、功能及作用机制研究进展显示文摘拓扑异构酶是存在于细胞核内的一类酶,它们能够催化DNA链的断裂和结合,从而调控DNA的拓扑状态,在基因复制、转录、重组、修复和染色体重塑过程中参与了DNA超螺旋结构模板的调节。拓扑异构酶通过催化切断DNA链的磷酸二酯键,产生DNA缺口而发挥作用,这种缺口可以改变DNA分子的拓扑结构,从而解决DNA缠结状态这一问题。在哺乳动物中,主要存在I型和II型两种拓扑异构酶。拓扑异构酶I(type I topoisomerase,Top1)催化产生DNA分子上的单链缺口,而拓扑异构酶II(type II topoisomerase,Top2)则催化产生DNA分子上的双链缺口。Top2在哺乳动物中又分为α亚型和β亚型。其中,Top2α的功能主要与细胞的增殖和多潜能性相关,而Top2β在神经发育中具有重要作用。本文就Top2的结构、功能和作用机制的相关研究进展作一综述。 | 秦尚尧 袁一旻 胡昕 孙秀 苏志达 | 2016 | 生理学报2016，68，1： | 6 |
| 7 | 脊髓损伤后胶质瘢痕形成的研究进展显示文摘脊髓损伤后,胶质瘢痕的形成主要涉及星形胶质细胞肥大、增殖、迁移以及表达的胶质纤维酸性蛋白、波形蛋白和巢蛋白的增加等多个过程,并且影响神经元轴突的生长。 | 巩朝阳 刘开鑫 向高 张海鸿 | 2018 | 中国康复理论与实践2018，24，6： | 5 |
| 8 | 亚低温对脊髓损伤后反应性星形胶质细胞增生的影响显示文摘目的:观察在不同温度条件下脊髓星形胶质细胞划痕损伤活化后的形态和活性改变,以探讨亚低温对脊髓损伤后反应性星形胶质细胞增生的影响。方法:体外原代培养新生SD大鼠脊髓星形胶质细胞,以划痕实验制备反应性星形胶质细胞。亚低温选择33℃,细胞培养48 h。实验分为对照组、划痕组、亚低温组和划痕+亚低温组。各组在相应的时间点观察细胞形态,采用免疫荧光染色方法检测Nestin阳性率,MTT比色法观察细胞活性,PI染色方法观察细胞凋亡程度。结果:与对照组和亚低温组相比,划痕组和划痕+亚低温组细胞胞体肥大,周围突起增多、延展以及胞浆丰富,细胞生长率明显升高。与划痕组相比,划痕+亚低温组细胞变化减慢,周围突起减少,细胞长入划痕处所需时间增加,细胞Nestin阳性率、PI阳性率和细胞生长率明显降低,各结果差异显著(P<0.01)。结论:划痕损伤后星形胶质细胞活化为反应性星形胶质细胞并会增生,亚低温明显抑制脊髓反应性星形胶质细胞的活化增生,并可以抑制星形胶质细胞的凋亡。 | 康文博 李晓红 陈翀 王景景 涂悦 张赛 梁海乾 | 2016 | 中国应用生理学杂志2016，32，4： | 5 |
| 9 | 脊髓损伤后硫酸软骨素蛋白多糖及GFAP表达的变化显示文摘目的探讨脊髓损伤后NG2、Neurocan、GFAP表达的变化。方法将32只雌性SD大鼠随机分为空白对照组和模型组。模型组采用脊髓横切法制作脊髓损伤模型,空白对照组仅切除T10全椎板及T9、T11部分椎板,对脊髓未作任何处理。分别在大鼠脊髓损伤制作后3、7、14及28 d时取材,利用免疫组织化学染色方法检测NG2、Neurocan、GFAP的表达情况。结果模型组脊髓损伤后3 d时NG2的表达出现明显升高,7 d时NG2的表达达到最高点,14 d及28 d时NG2仍然维持在较高水平,但与7 d时的表达相比有下降,空白对照组NG2各时间点均呈低表达。模型组脊髓损伤后7 d时Neurocan的表达显著增加,于14 d时达到最高点,从14 d开始Neurocan的表达开始逐步下降,空白对照组Neurocan各时间点均呈低表达。模型组脊髓损伤后3 d时GFAP的表达明显升高,14 d时GFAP的表达达到顶点,28 d时损伤部位GFAP的表达均较空白对照组明显升高,两组比较差异有统计学意义(均P<0.05)。结论脊髓损伤后NG2、Neurocan、GFAP表达升高,可能是脊髓损伤后抑制轴突再生的因素之一。 | 王国毓 程志坚 杨保辉 李浩鹏 贺西京 | 2020 | 生物骨科材料与临床研究2020，17，1： | 4 |
| 10 | 脊髓损伤后室管膜区内源性神经干细胞反应的系列问题显示文摘背景:脊髓损伤是中枢神经系统的严重损伤,目前尚未有一种有效的方法可以将其治愈。脊髓损伤患者在生理和心理上都承受巨大的痛苦,而高昂的治疗费用以及严重的后遗症,已成为患病家庭的主要负担。随着对内源性神经干细胞分子生物学研究的不断发展,研究发现利用内源性神经干细胞修复受损脊髓传导束有巨大潜力,这也为重建功能神经环路带来了希望。目的:综述脊髓损伤后内源性神经干细胞如何反应及其调控因素。方法:检索PubMed、Web of Science数据库及万方、CNKI中国期刊全文数据库收录的脊髓损伤后内源性神经干细胞反应的相关文章,英文检索词为“spinal cord injury,endogenous neural stem cell”,中文检索词为“脊髓损伤,内源性神经干细胞”,按纳入和排除标准共纳入70篇文献进行归纳总结。结果与结论:脊髓损伤后室管膜区的内源性神经干细胞被激活,迁移至受损部位,分化为功能性神经元及胶质细胞,限制损伤进一步扩大,修复受损的神经结构,这一过程受到了继发性脊髓损伤时释放的多种因子的影响,而对于内源性神经干细胞的来源及其被激活的机制,以及如何诱导其向更利于修复脊髓损伤的方向分化仍需要更深一步的研究。 | 范一鸣 刘方煜 张洪宇 李帅 王岩松 | 2022 | 中国组织工程研究2022，26，7： | 4 |
| 11 | Molecular approaches for spinal cord injury treatment显示文摘Injuries to the spinal cord result in permanent disabilities that limit daily life activities.The main reasons for these poor outcomes are the limited regenerative capacity of central neurons and the inhibitory milieu that is established upon traumatic injuries.Despite decades of research,there is still no efficient treatment for spinal cord injury.Many strategies are tested in preclinical studies that focus on ameliorating the functional outcomes after spinal cord injury.Among these,molecular compounds are currently being used for neurological recovery,with promising results.These molecules target the axon collapsed growth cone,the inhibitory microenvironment,the survival of neurons and glial cells,and the re-establishment of lost connections.In this review we focused on molecules that are being used,either in preclinical or clinical studies,to treat spinal cord injuries,such as drugs,growth and neurotrophic factors,enzymes,and purines.The mechanisms of action of these molecules are discussed,considering traumatic spinal cord injury in rodents and humans. | Fernanda Martins de Almeida Suelen Adriani Marques Anne Caroline Rodrigues dos Santos Caio Andrade Prins Fellipe Soares dos Santos Cardoso Luiza dos Santos Heringer Henrique Rocha Mendonça Ana Maria Blanco Martinez | 2023 | Neural Regeneration Research2023，18，1： | 3 |
| 12 | Scar-modulating treatments for central nervous system injury显示文摘Traumatic injury to the adult mammalian central nervous system(CNS) leads to complex cellular responses. Among them, the scar tissue formed is generally recognized as a major obstacle to CNS repair, both by the production of inhibitory molecules and by the physical impedance of axon regrowth. Therefore, scar-modulating treatments have become a leading therapeutic intervention for CNS injury. To date, a variety of biological and pharmaceutical treatments, targeting scar modulation, have been tested in animal models of CNS injury, and a few are likely to enter clinical trials. In this review, we summarize current knowledge of the scar-modulating treatments according to their specific aims:(1) inhibition of glial and fibrotic scar formation, and(2) blockade of the production of scar-associated inhibitory molecules. The removal of existing scar tissue is also discussed as a treatment of choice. It is believed that only a combinatorial strategy is likely to help eliminate the detrimental effects of scar tissue on CNS repair. | Dingding Shen Xiaodong Wang Xiaosong Gu | 2014 | Neuroscience Bulletin2014，30，6： | 3 |
| 13 | The therapeutic potential of targeting exchange protein directly activated by cyclic adenosine 3',5'-monophosphate(Epac)for central nervous system trauma显示文摘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. | Alba Guijarro-Belmar Dominik Mateusz Domanski Xuenong Bo Derryck Shewan Wenlong Huang | 2021 | Neural Regeneration Research2021，16，3： | 3 |
| 14 | 依达拉奉干预脊髓损伤模型大鼠Ⅰ型和Ⅳ型胶原蛋白的表达显示文摘背景:依达拉奉是一种有效的氧自由基清除剂,有研究报道其可以有效改善脊髓损伤后肢体运动功能,但是其对损伤组织修复的作用机制尚不明确。目的:通过观察脊髓损伤后大鼠肢体功能评分的变化及Ⅰ型胶原蛋白和Ⅳ型胶原蛋白表达情况,探讨依达拉奉促进脊髓损伤大鼠肢体功能恢复的机制。方法:将36只大鼠随机分为3组,每组12只:假手术组不损伤脊髓,仅去除椎板后缝合+生理盐水腹腔注射;模型组去除椎板后行NYU脊髓打击器建立脊髓损伤模型+腹腔注射生理盐水;依达拉奉组:去除椎板后行NYU脊髓打击器建立脊髓损伤模型+腹腔注射依达拉奉。造模后第1天开始进行药物干预,持续7 d。干预后1,3,5及7 d对各组大鼠进行Basso Beattie Bresnahan(BBB)肢体功能评分;干预后第7天,处死大鼠,取出脊髓,尼式染色观察脊髓神经元细胞的形态;免疫组化法和Western blot检测Ⅰ型和Ⅳ型胶原蛋白表达情况。结果与结论:(1)与模型组相比,干预第5天后,依达拉奉组的BBB评分显著升高(P<0.05);(2)尼式染色显示假手术组脊髓灰白质界限清晰,神经细胞胞质内可见较大且明显的核仁;依达拉奉组,细胞形态较为完整,细胞水肿较轻,瘀血面积较小;模型组神经元细胞空洞较多且大,细胞核肿胀,甚至出现核仁消失的情况;(3)Western blot和免疫组化实验结果显示依达拉奉组的Ⅰ型胶原蛋白和Ⅳ型胶原蛋白表达水平显著高于模型组多(P<0.05);(4)结果提示,依达拉奉对脊髓损伤后大鼠的肢体功能障碍有显著改善作用,可能与增加Ⅰ型胶原蛋白和Ⅳ型胶原蛋白的表达有关。 | 李仁斌 余光书 林焱斌 周家烽 黄奕祺 郑伟 | 2018 | 中国组织工程研究2018，22，8： | 3 |
| 15 | 脊髓损伤患者大脑中央前回的代谢改变显示文摘目的观察脊髓损伤患者大脑中央前回初级运动皮质(M1)代谢变化。方法 2018年12月至2019年10月,选择住院脊髓损伤患者20例(患者组)和健康人15例(对照组),使用磁共振波谱(MRS)观察大脑左侧M1感兴趣区氮-乙酰天门冬氨酸(NAA)、胆碱(Cho)、肌酸(Cr)和肌醇(MI)浓度。结果患者组MI浓度较对照组明显增高(t=3.745, P <0.01),NAA、Cho、Cr、NAA/Cr、Cho/Cr、Cho/NAA与对照组相比无显著性差异(t <1.431, P> 0.05)。结论脊髓损伤患者M1区可能有胶质细胞增生,提示发生代偿性修复。 | 李雅静 李建军 高峰 郭韵 刘俊 徐珮珮 | 2020 | 中国康复理论与实践2020，26，4： | 2 |
| 16 | 脊髓损伤模型大鼠鞘内注射甲基强的松龙后的蛋白质组学变化显示文摘背景:临床研究表明,早期使用甲基强的松龙可以促进损伤神经功能恢复,合理的初始剂量、剂量间隔时间和治疗持续时间是甲基强的松龙治疗急性脊髓损伤取得良好效果的关键。目的:观察急性脊髓损伤模型大鼠鞘内注射大剂量甲基强的松龙后的脊髓组织差异蛋白表达质谱。方法:取8只SD大鼠,建立急性脊髓损伤模型,随机分2组,分别于造模后0,8 h鞘内注射甲基强的松龙7.5 mg/kg,于注射24 h后取损伤段脊髓组织,采用同位素标记相对和绝对定量技术分析两组差异蛋白质及表达明显相关神经再生的差异蛋白。结果与结论:共鉴定到了87个差异表达的蛋白,与0 h组相比,8 h组上调的差异蛋白有43个,下调的差异蛋白数是44个。相关神经再生的差异蛋白18个,上调的差异蛋白有8个,下调的差异蛋白数是10个,其中OMgp是一个潜在的神经轴突生长抑制因子,OMgp与Ng R/P75/TROY/Lingo-1组成受体复合体特异性结合,通过第二信使c AMP激活Rho A作用可抑制轴突生长锥的崩解。提示鉴定鞘内注射甲基强的松龙治疗大鼠急性脊髓损伤后脊髓差异蛋白和脊髓相关神经再生因子,分别进行蛋白数据库检索和功能分析,其表达可能作为急性脊髓损伤后临床上监测神经损伤再生的指标。 | 杨贝贝 陈江涛 宋兴华 | 2014 | 中国组织工程研究2014，18，49： | 2 |
| 17 | Bioinformatic identification of key candidate genes and pathways in axon regeneration after spinal cord injury in zebrafish显示文摘Zebrafish and human genomes are highly homologous;however,despite this genomic similarity,adult zebrafish can achieve neuronal proliferation,regeneration and functional restoration within 6–8 weeks after spinal cord injury,whereas humans cannot.To analyze differentially expressed zebrafish genes between axon-regenerated neurons and axon-non-regenerated neurons after spinal cord injury,and to explore the key genes and pathways of axonal regeneration after spinal cord injury,microarray GSE56842 was analyzed using the online tool,GEO2R,in the Gene Expression Omnibus database.Gene ontology and protein-protein interaction networks were used to analyze the identified differentially expressed genes.Finally,we screened for genes and pathways that may play a role in spinal cord injury repair in zebrafish and mammals.A total of 636 differentially expressed genes were obtained,including 255 up-regulated and 381 down-regulated differentially expressed genes in axon-regenerated neurons.Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment results were also obtained.A protein-protein interaction network contained 480 node genes and 1976 node connections.We also obtained the 10 hub genes with the highest correlation and the two modules with the highest score.The results showed that spectrin may promote axonal regeneration after spinal cord injury in zebrafish.Transforming growth factor beta signaling may inhibit repair after spinal cord injury in zebrafish.Focal adhesion or tight junctions may play an important role in the migration and proliferation of some cells,such as Schwann cells or neural progenitor cells,after spinal cord injury in zebrafish.Bioinformatic analysis identified key candidate genes and pathways in axonal regeneration after spinal cord injury in zebrafish,providing targets for treatment of spinal cord injury in mammals. | Jia-He Li Zhong-Ju Shi Yan Li Bin Pan Shi-Yang Yuan Lin-Lin Shi Yan Hao Fu-Jiang Cao Shi-Qing Feng | 2020 | Neural Regeneration Research2020，15，1： | 2 |
| 18 | Neuroprotective role of Noggin in spinal cord injury显示文摘Spinal cord injury is one of the leading causes of morbidity and mortality among young adults in many countries including the United States.Difficulty in the regeneration of neurons is one of the main obstacles that leave spinal cord injury patients with permanent paralysis in most instances.Recent research has found that preventing acute and subacute secondary cellular damages to the neurons and supporting glial cells can help slow the progression of spinal cord injury pathogenesis,in part by reactivating endogenous regenerative proteins including Noggin that are normally present during spinal cord development.Noggin is a complex protein and natural inhibitor of the multifunctional bone morphogenetic proteins,and its expression is high during spinal cord development and after induction of spinal cord injury.In this review article,we first discuss the change in expression of Noggin during pathogenesis in spinal cord injury.Second,we discuss the current research knowledge about the neuroprotective role of Noggin in preclinical models of spinal cord injury.Lastly,we explain the gap in the knowledge for the use of Noggin in the treatment of spinal cord injury.The results from extensive in vitro and in vivo research have revealed that the therapeutic efficacy of Noggin treatment remains debatable due to its neuroprotective effects observed only in early phases of spinal cord injury but little to no effect on altering pathogenesis and functional recovery observed in the chronic phase of spinal cord injury.Furthermore,clinical information regarding the role of Noggin in the alleviation of progression of pathogenesis,its therapeutic efficacy,bioavailability,and safety in human spinal cord injury is still lacking and therefore needs further investigation. | Nadia Al-Sammarraie Mohammed Mahmood Swapan K.Ray | 2023 | Neural Regeneration Research2023，18，3： | 2 |
| 19 | 过表达NeuroD1对脊髓反应性星形胶质细胞转分化为神经元的影响显示文摘目的探讨过表达Neuro D1对脊髓反应性星形胶质细胞转分化为神经元的影响。方法体外原代培养SD大鼠脊髓星形胶质细胞,以划痕实验制备反应性星形胶质细胞。实验分为空白组(NV组)、对照病毒组(GFP组)和Neuro D1病毒组(Neuro D1组)。各组行划痕处理7 d后,NV组不感染病毒,GFP组感染携带GFP基因的逆转录病毒,Neuro D1组感染同时携带GFP和Neuro D1基因的逆转录病毒,24 h后同时更换神经元条件培养基。各组在1 d、2 d、3 d、5 d、7 d、14 d观察细胞形态,并采用免疫荧光染色方法分别在感染病毒后7 d观察细胞DCX阳性率和14 d观察细胞Neu N阳性率。结果更换神经元条件培养基后,各组细胞形态发生改变,胞核明显饱满,胞浆减少,突起减少并延长。与Neuro D1组相比,NV组和GFP组细胞突起短而分枝多,胞核较小。感染病毒后7 d,NV组和GFP组细胞部分形态逐渐恢复以前形态而Neuro D1组维持变化后形态。与NV组和GFP组相比,Neuro D1组出现DCX(9.84%±2.06%)(F=40.107)和Neu N(8.25%±2.78%)阳性细胞(F=21.73),结果差异都有统计学意义(P<0.05)。结论在体外培养,Neuro D1的过表达可以介导体外培养脊髓反应性星形胶质细胞转分化为神经元。 | 康文博 陈翀 李晓红 王景景 涂悦 张赛 梁海乾 | 2015 | 中国神经精神疾病杂志2015，41，9： | 1 |
| 20 | Targeting ERK1/2-calpain 1-NF-κB signal transduction in secondary tissue damage and astrogliosis after spinal cord injury显示文摘Neuronal 损坏, glial 发炎,和 astrogliosis/astroglial 疤形成是是到在针的绳索损害(SCI ) 以后的功能的赤字的重要贡献者的主要第二等的损害机制。学习的目的是处于织物损坏和在老鼠跟随 SCI 的 astrogliosis/astroglial 疤形成评估 ERK2 对 ERK1/2 和 ERK1/2-calpain 1NF-B 信号 transduction 的不同角色。RNAi 途径,药理学干预(U0126 ) ,西方的污点分析, immunofluorescence 分析,和组织学的评价被用来为 neuroprotection 指向 ERK1/2-calpain 1-NF-B 信号 transduction 小径。组织学的染色分析有选择地表明了那与 U0126 用 pERK1/2 的 ERK2 siRNA,然而并非抑制减少 pERK2,显著地减少了损害体积并且改进了全部的织物 sparing,白事 sparing,和灰色的物质在针的绳索的 sparing 在 contusive SCI 以后的二个星期。一条 ERK1/2-calpain 1-NF-B 信号 transduction 小径在 SCI 以后涉及 astroglial 疤形成。由 U0126 的 ERK1/2 的封锁减少了 calpain 1 表情 4 h 追随者 SCI。由 lentiviral shRNA 的 1 减小稀释了的选择 calpain 在在老鼠的 SCI 以后的 astroglial NF-B 活动和 astroglial 疤形成。一起拿,这些结果表明处于织物损坏和 astrogliosis/astroglial 的 1 个发信号小径留下疤痕的单个 ERK2 和 calpain 的参与在 SCI 的动物模型的形成。因此,指向单个英皇家空军之阶级最低之兵和它 calpain 1-NF-B 的下游的信号 transduction 可以为最小化织物损坏和 astroglial 疤形成追随者 SCI 作为新奇治疗学提供更大的潜力。 | Xin Xin Yu Vimala Bondada Colin Rogers Carolyn A. Meyer Chen Guang Yu | 2015 | Frontiers in Biology2015，10，5： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员