Salvianolic acid B protects the myelin sheath around injured spinal cord axons

Salvianolic acid B,an active pharmaceutical compound present in Salvia miltiorrhiza,exerts a neuroprotective effect in animal models of brain and spinal cord injury.Salvianolic acid B can promote recovery of neurological function;however,its protective effect on the myelin sheath after spinal cord injury remains poorly understood.Thus,in this study,in vitro tests showed that salvianolic acid B contributed to oligodendrocyte precursor cell differentiation,and the most effective dose was 20 μg/m L.For in vivo investigation,rats with spinal cord injury were intraperitoneally injected with 20 mg/kg salvianolic acid B for 8 weeks.The amount of myelin sheath and the number of regenerating axons increased,neurological function recovered,and caspase-3 expression was decreased in the spinal cord of salvianolic acid B-treated animals compared with untreated control rats.These results indicate that salvianolic acid B can protect axons and the myelin sheath,and can promote the recovery of neurological function.Its mechanism of action is likely to be associated with inhibiting apoptosis and promoting the differentiation and maturation of oligodendrocyte precursor cells.

Research advances in experiments on correlation between schizophrenia and myelin sheath abnormality

Schizophrenia,as a common mental disease,seriously threatens the physical and mental health of human beings.It is characterized by many mental and behavioral disorders,such as uncoordinated thinking and emotional mode which separated from the actual living environment.Patients with schizophrenia are prone to relapse and deterioration due to their long course of disease,resulting in the loss of labor force.It has been proved that the occurrence and development of schizophrenia is closely related to the abnormal development of oligodendrocytes,which have the function of myelin formation and the dysfunction of myelin sheath itself.For a comprehensive understanding of myelin abnormal effects on the pathogenesis of schizophrenia,this paper is to review the literature,then summarize and discuss the animal experimental literature related to the abnormal myelin sheath in schizophrenia from the perspectives of behavioristics,neuroimaging,protein expression and stereology,in order to further clarify the influence of the abnormal myelin sheath on the pathogenesis of schizophrenia and provide ideas for the diagnosis of schizophrenia and the research and development of new drugs.

Human umbilical cord Wharton's jelly-derived oligodendrocyte precursor-like cells for axon and myelin sheath regeneration

Human umbilical mesenchymal stem cells from Wharton's jelly of the umbilical cord were induced to differentiate into oligodendrocyte precursor-like cells in vitro. Oligodendrocyte precursor cells were transplanted into contused rat spinal cords. Immunofluorescence double staining indicated that transplanted cells survived in injured spinal cord, and differentiated into mature and immature oligodendrocyte precursor cells. Biotinylated dextran amine tracing results showed that cell transplantation promoted a higher density of the corticospinal tract in the central and caudal parts of the injured spinal cord. Luxol fast blue and toluidine blue staining showed that the volume of residual myelin was significantly increased at 1 and 2 mm rostral and caudal to the lesion epicenter after cell transplantation. Furthermore, immunofluorescence staining verified that the newly regenerated myelin sheath was derived from the central nervous system. Basso, Beattie and Bresnahan testing showed an evident behavioral recovery. These results suggest that human umbilical mesenchymal stem cell-derived oligodendrocyte precursor cells promote the regeneration of spinal axons and myelin sheaths.

Direct contacts of microglia on myelin sheath and Ranvier’s node in the corpus callosum in rats

Over the recent years, it has been found that microglia pseudopodia contact synapses, detect sick ones and prune them, even in adult animals. Myelinated nerves also carry out plasticity in which microglia remove myelin debris by phagocytosis. However, it remains unknown whether microglia explore structures on nerve fibers, such as Ranvier’s node(RN) or myelin sheath, before they become debris. By double or triple staining RNs or myelin sheathes and microglia in healthy rat corpus callosum, this study unveiled direct contacts of microglia pseudopodia with RNs and with para-and inter-nodal myelin sheathes, which was then verified by electron microscopic observations. Our data indicated that microglia also explore unmyelinated nerve fibers. Furthermore, we used the animals with matured white matter;therefore, microglia may be actively involved in plasticity of matured white matter tracts as it does for synapse pruning, instead of only passively phagocytize myelin debris.

Stereological method for objectively quantifying myelin sheaths in the rat hippocampus

In the present study,tissue blocks were randomly sampled from the entire hippocampus of 6-week-old Long-Evans rats.Isotropic,uniform and random sections,60 nm thick,were prepared by isector.Fifteen fields of view were randomly selected for each section and photographed using a transmission electron microscope.The mean internal and external diameters of the myelin sheaths were obtained by measuring the longest profile diameter perpendicular to its longest axis.The inner and outer perimeters of the myelin sheaths were estimated using the equidistant parallel test lines.The thickness of the myelin sheaths was estimated by direct orthogonal measurements in uniform,random locations.These stereological methods should permit an unbiased quantitative assessment of changes in the myelin sheaths of myelinated fibers in the hippocam-pus.

Cell vibron polariton resonantly self-confined in the myelin sheath of nerve

Polaritons are arousing tremendous interests in physics and material sciences for their unique and amazing properties,especially including the condensation,lasing without inversion and even room-temperature superfluidity.Herein,we propose a cell vibron polariton(cell-VP):a collectively coherent mode of a photon and all phospholipid molecules in a myelin sheath formed by glial cells.Cell-VP can be resonantly self-confined in the myelin sheath under physiological conditions.The observations benefit from the specifically compact,ordered and polar thin-film structure of the sheath,and the relatively strong coupling of the mid-infrared photon with the vibrons of phospholipid tails in the myelin.The underlying physics is revealed to be the collectively coherent superposition of the photon and vibrons,the polariton induced significant enhancement of myelin permittivity,and the resonance of the polariton with the sheath.The captured cell-VPs in myelin sheaths may provide a promising way for super-efficient consumption of extra-weak bioenergy and even directly serve for quantum information.These findings further the understanding of nervous system operations at cellular level from the view of quantum mechanics.

Insights into myelin dysfunction in schizophrenia and bipolar disorder

Schizophrenia and bipolar disorder are disabling psychiatric disorders with a worldwide prevalence of approximately 1%.Both disorders present chronic and deteriorating prognoses that impose a large burden,not only on patients but also on society and health systems.These mental illnesses share several clinical and neurobiological traits;of these traits,oligodendroglial dysfunction and alterations to white matter(WM)tracts could underlie the disconnection between brain regions related to their symptomatic domains.WM is mainly composed of heavily myelinated axons and glial cells.Myelin internodes are discrete axon-wrapping membrane sheaths formed by oligodendrocyte processes.Myelin ensheathment allows fast and efficient conduction of nerve impulses through the nodes of Ranvier,improving the overall function of neuronal circuits.Rapid and precisely synchronized nerve impulse conduction through fibers that connect distant brain structures is crucial for higher-level functions,such as cognition,memory,mood,and language.Several cellular and subcellular anomalies related to myelin and oligodendrocytes have been found in postmortem samples from patients with schizophrenia or bipolar disorder,and neuroimaging techniques have revealed consistent alterations at the macroscale connectomic level in both disorders.In this work,evidence regarding these multilevel alterations in oligodendrocytes and myelinated tracts is discussed,and the involvement of proteins in key functions of the oligodendroglial lineage,such as oligodendrogenesis and myelination,is highlighted.The molecular components of the axo-myelin unit could be important targets for novel therapeutic approaches to schizophrenia and bipolar disorder.

Lgi1基因通过控制髓鞘装配和TSC1-mTORC1依赖的脂质生物合成促进外周神经系统髓鞘化

目的 探索富亮氨酸胶质瘤失活基因1(Lgi1)在外周神经系统(PNS)髓鞘化的作用及其分子机制。方法 应用蛋白质印迹法检测Lgi1与髓鞘相关蛋白在产后发育时期SN组(坐骨神经)P3-P60、Brain组(大脑)P0-P180、敲除Lgi1后SN组与Brain组的表达,并进一步探索Lgi1-/-小鼠Laminin-integrin信号及TSC1-mTORC1通路相关蛋白表达情况;利用免疫组织化学与电镜探究敲除Lgi1后引起的髓鞘超微结构改变。结果 蛋白质印迹法显示,Lgi1的缺失会导致PNS中髓鞘相关蛋白MBP、MOG和MAG与特异性髓鞘蛋白MPZ的表达水平下降(P<0.05),且电镜下实验组小鼠SN中无髓鞘的轴突数量增加,而轴突总数不变,g-ratio比率增加,且未折叠髓鞘增加;Lgi1-/-小鼠SN中Laminin、integrinβ-1、integrinβ-4蛋白表达明显减少,integrin α-1表达增加(P<0.05);免疫荧光染色结果显示,MBP与Laminin共染部分较少;此外,与对照组相比,Lgi1-/-小鼠中脂肪酸合成酶FASN蛋白表达量减少,pS6水平增加和TSC1表达减少(P<0.05)。结论 Lgi1基因参与调控PNS髓鞘化过程,且通过Laminin-integrin信号及TSC1-mTORC1通路抑制髓鞘的形成并导致PNS低髓鞘化。

Rosmarinic acid ameliorates hypoxia/ischemia induced cognitive deficits and promotes remyelination

Rosmarinic acid,a common ester extracted from Rosemary,Perilla frutescens,and Salvia miltiorrhiza Bunge,has been shown to have protective effects against various diseases.This is an investigation into whether rosmarinic acid can also affect the changes of white matter fibers and cognitive deficits caused by hypoxic injury.The right common carotid artery of 3-day-old rats was ligated for 2 hours.The rats were then prewarmed in a plastic container with holes in the lid,which was placed in 37°C water bath for 30 minutes.Afterwards,the rats were exposed to an atmosphere with 8% O2 and 92% N2 for 30 minutes to establish the perinatal hypoxia/ischemia injury models.The rat models were intraperitoneally injected with rosmarinic acid 20 mg/kg for 5 consecutive days.At 22 days after birth,rosmarinic acid was found to improve motor,anxiety,learning and spatial memory impairments induced by hypoxia/ischemia injury.Furthermore,rosmarinic acid promoted the proliferation of oligodendrocyte progenitor cells in the subventricular zone.After hypoxia/ischemia injury,rosmarinic acid reversed to some extent the downregulation of myelin basic protein and the loss of myelin sheath in the corpus callosum of white matter structure.Rosmarinic acid partially slowed down the expression of oligodendrocyte marker Olig2 and myelin basic protein and the increase of oligodendrocyte apoptosis marker inhibitors of DNA binding 2.These data indicate that rosmarinic acid ameliorated the cognitive dysfunction after perinatal hypoxia/ischemia injury by improving remyelination in corpus callosum.This study was approved by the Animal Experimental Ethics Committee of Xuzhou Medical University,China (approval No.20161636721) on September 16,2017.

A quantitative study on changes of the myelinated fibers in the cerebral cortex of cortical dysplasia rats

An animal model of cortical dysplasia was established through X-ray irradiation induced subcortical heterotopic nodules in rats. Transmission electron microscopy detection of the ultrastructure and the stereology examination showed that there was a significant decrease in cerebral white matter and hippocampal volume, the total volume, volume density, length density and total length of the myelinated fibers in the white matter of cortical dysplasia rats. Subcortical heterotopic nodules of the hippocampal CA1 region and synaptic number density in the CA3 region were reduced compared with normal rats. Our experimental findings indicate that erosed subcortical heterotopic nodules, decreased total length of myelinated nerve fibers and demyelination directly lead to a reduction of white matter volume.

Axonal damage in myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalomyelitis in a C57BL/6 mouse model may be not secondary to inflammatory demyelination

The present study established a chronic experimental autoimmune encephalomyelitis model in C57BL/6 mice induced by myelin oligodendrocyte glycoprotein peptides and complete Freund's adjuvant.Onset latency was 12 days,with an incidence rate of 100%.Neuropathological characteristics included perivascular inflammatory cell infiltration,demyelination,neuronal degeneration,and axonal damage within cerebral and myelic white matter.Electron microscopy revealed swollen mitochondria,complete organ disappearance,and fused or broken myelin sheath structure,which were accompanied by myelin sheath reconstruction.Moreover,axonal damage was not consistent with demyelination distribution,and severity of axonal damage did not correlate with demyelination.Results suggested that axonal damage in an experimental autoimmune encephalomyelitis model is not secondary to inflammatory demyelination.

Action potential-simulated weak electric fields can directly initiate myelination

BACKGROUND: Myelination is a process whereby glial cells identify, adhere, wrap and enclose axons to form a spiral myelin sheath. OBJECTIVE: To investigate the effects of action potential-simulated weak electric fields on myelination in the central nervous system. DESIGN AND SETTING: This single-sample observation study was performed at the 324 Hospital of Chinese PLA. MATERIALS: Two 5 μm carbon fibers were provided by the Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. One Sprague Dawley rat, aged 1 day, was used. METHODS: Cerebral cortex was harvested from the rat to prepare a suspension [(1-2)×105/mL] containing neurons and glial cells. To simulate the axon, carbon fibers were placed at the bottom of the neuron-glial cell coculture dish, and were electrified with a single phase square wave current, 1×10-2, 1×10-3, 1×10-4, and 1×10-5 seconds, 1 Hz, 40 mV, and 10 μA, 30 minutes each, once a day for 10 consecutive days to simulate weak negative electric fields during action potential conduction. MAIN OUTCOME MEASURES: Glial cell growth and wrapping of carbon fibers were observed by phase contrast microscopy and immunohistochemistry. RESULTS: On culture day 7, cell groups were found to adhere to negative carbon fibers in the 1×10-3 seconds square wave group. Cell membrane-like substances grew out of cell groups, wrapped the carbon fibers, and stretched to the ends of carbon fibers. Only some small and round cells close to negative carbon fibers were found on culture day 12. In the 1×10-4 and 1×10-3 seconds square wave groups, the negative carbon fibers were wrapped by oligodendrocytes or their progenitor cells. CONCLUSION: The local negative electric field which is generated by action potentials at 1×(10-4-10-3) seconds, 40 mV can directly initiate and participate in myelination in the central nervous system.

A hyaluronic acid granular hydrogel nerve guidance conduit promotes regeneration and functional recovery of injured sciatic nerves in rats

A hyaluronic acid granular hydrogel can promote neuronal and astrocyte colony formation and axonal extension in vitro,suggesting that the hydrogel can simulate an extracellular matrix structure to promote neural regeneration.However,in vivo experiments have not been conducted.In this study,we transplanted a hyaluronic acid granular hydrogel nerve guidance conduit to repair a 10-mm long sciatic nerve gap.The Basso,Beattie,and Bresnahan locomotor rating scale,sciatic nerve compound muscle action potential recording,Fluoro-Gold retrograde tracing,growth related protein 43/S100 immunofluorescence staining,transmission electron microscopy,gastrocnemius muscle dry/wet weight ratio,and Masson’s trichrome staining results showed that the nerve guidance conduit exhibited similar regeneration of sciatic nerve axons and myelin sheath,and recovery of the electrophysiological function and motor function as autologous nerve transplantation.The conduit results were superior to those of a bulk hydrogel or silicone tube transplant.These findings suggest that tissue-engineered nerve conduits containing hyaluronic acid granular hydrogels effectively promote the morphological and functional recovery of the injured sciatic nerve.The nerve conduits have the potential as a material for repairing peripheral nerve defects.

Serum response factor promotes axon regeneration following spinal cord transection injury

Studies have snown that serum response factor is beneficaial for axonar regeneration of peripheral herves.However,Its role after central nervous system injury remains unclear. In this study,we established a rat model of T9-T10 spinal cord transection injury.We found that the expression of serum response factor in injured spinal cord gray matter neurons gradually increased with time,reached its peak on the 7^(th) day,and then gradually decreased.To investigate the role of serum response factor,we used lentivirus vecto rs to ove rexpress and silence serum response factor in spinal cord tissue.We found that overexpression of serum response factor promoted motor function recovery in rats with spinal cord injury.Qualitative observation of biotinylated dextran amine anterograde tra cing showed that ove rexpression of serum response factor increased nerve fibers in the injured spinal co rd.Additionally,transmission electron microscopy showed that axon and myelin sheath morphology was restored.Silencing serum response factor had the opposite effects of ove rexpression.These findings suggest that serum response factor plays a role in the recovery of motor function after spinal cord injury.The underlying mechanism may be related to the regulation of axonal regeneration.

Reduced graphene oxide-embedded nerve conduits loaded with bone marrow mesenchymal stem cell-derived extracellular vesicles promote peripheral nerve regeneration

We previously combined reduced graphene oxide(rGO)with gelatin-methacryloyl(GelMA)and polycaprolactone(PCL)to create an rGO-GelMA-PCL nerve conduit and found that the conductivity and biocompatibility were improved.However,the rGO-GelMA-PCL nerve conduits differed greatly from autologous nerve transplants in their ability to promote the regeneration of injured peripheral nerves and axonal sprouting.Extracellular vesicles derived from bone marrow mesenchymal stem cells(BMSCs)can be loaded into rGO-GelMA-PCL nerve conduits for repair of rat sciatic nerve injury because they can promote angiogenesis at the injured site.In this study,12 weeks after surgery,sciatic nerve function was measured by electrophysiology and sciatic nerve function index,and myelin sheath and axon regeneration were observed by electron microscopy,immunohistochemistry,and immunofluorescence.The regeneration of microvessel was observed by immunofluorescence.Our results showed that rGO-GelMA-PCL nerve conduits loaded with BMSC-derived extracellular vesicles were superior to rGO-GelMA-PCL conduits alone in their ability to increase the number of newly formed vessels and axonal sprouts at the injury site as well as the recovery of neurological function.These findings indicate that rGO-GelMA-PCL nerve conduits loaded with BMSC-derived extracellular vesicles can promote peripheral nerve regeneration and neurological function recovery,and provide a new direction for the curation of peripheral nerve defect in the clinic.

沉默海马LINGO-1对小鼠学习记忆以及有髓神经纤维的影响

目的:研究沉默海马含亮氨酸重复序列和免疫球蛋白结构域的蛋白-1(LINGO-1)对APP/PS1小鼠空间学习和记忆能力以及海马有髓神经纤维的影响。方法:随机选取18只雄性APP/PS1小鼠,随机分为对照组和rAAV-LINGO-1-shRNA组,通过海马立体定位注射表达LINGO-1-shRNA的重组腺相关病毒rAAV-LINGO-1-shRNA,运用Morris水迷宫方法测试小鼠的空间学习和记忆能力;运用免疫荧光染色和real time RT-PCR分析小鼠海马内LINGO-1表达水平;运用real time RT-PCR分析小鼠海马内LINGO-1下游分子RhoA和ROCK的表达水平;运用无偏体视学方法结合透射电子显微镜技术对小鼠海马(CA1~3和齿状回)的体积,海马内有髓神经纤维的长度、髓鞘体积及其损伤情况进行定量研究。结果:与对照组小鼠相比,rAAV-LINGO-1-shRNA组小鼠的逃避潜伏期显著性缩短,穿台次数显著增多,而目标象限游泳时间及目标象限游泳路程比无显著性改变;与对照组相比,rAAV-LINGO-1-shRNA组海马内LINGO-1显著下调,同时其下游RhoA和ROCK的表达水平降低;对照组和rAAV-LINGO-1-shRNA组海马体积无显著性差异;与对照组相比,rAAV-LINGO-1-shRNA组海马内有髓神经纤维的长度和正常髓鞘的体积显著性增加,受损的有髓神经纤维占比和受损的髓鞘占比均显著降低。结论:沉默海马LINGO-1能够有效改善APP/PS1小鼠海马依赖的空间学习和记忆能力,抑制RhoA/ROCK的表达,减轻海马内有髓神经纤维及其髓鞘的损伤,这将为阿尔茨海默病的发病及治疗提供新的方向。

神经胶质抗原2胶质细胞与中枢神经系统疾病的研究进展

神经胶质抗原2(NG2)胶质细胞是兼具神经元和胶质细胞特性的特殊细胞,其细胞表面特异性表达NG2硫酸软骨素蛋白多糖。NG2胶质细胞是脑内区别于神经元、成熟少突胶质细胞、星形胶质细胞和小胶质细胞的细胞亚群,广泛存在于发育和成年的哺乳动物中枢神经系统(CNS)中,参与调节CNS的重建、神经网络、轴突生长和多种CNS疾病。CNS失衡在帕金森病、阿尔茨海默病等神经系统疾病的发病机制中发挥重要作用。因此,深入研究NG2与CNS疾病的相关性,可以为疾病的治疗提供新思路。

THIP对MK-801介导小鼠脑脱髓鞘损伤的保护作用

目的 探究γ-氨基丁酸(GABA)A受体(GABAAR)选择性激动剂加波沙朵(THIP)对地卓西平马来酸盐(MK-801)介导小鼠脑髓鞘损伤后小鼠认知障碍、髓鞘损伤和少突胶质细胞(OLs)分化的保护作用。方法 将36只C57BL/6J小鼠随机分为对照组(Blank组)、MK-801损伤组(MK-801组)和THIP干预组(MK-801+THIP组),每组12只。采用腹腔注射MK-801的方法制备MK-801脑损伤模型,MK-801组小鼠连续14 d腹腔注射MK-801,MK-801+THIP组小鼠在第8天添加THIP直至造模结束,Blank组腹腔注射相同剂量生理盐水。利用水迷宫实验检测小鼠学习记忆功能的改变;电镜观察髓鞘超微结构的改变;免疫荧光实验检测成熟少突胶质细胞(OLs)(CC-1+/Olig2+)数量的改变;利用Western blot检测少突胶质细胞分化调控蛋白GPR17的改变。结果 水迷宫实验结果显示,MK-801组小鼠学习记忆功能受损,MK-801+THIP组小鼠学习记忆功能有改善(P均<0.05);电镜结果显示,MK-801组小鼠髓鞘板层结构松散,MK-801+THIP组小鼠髓鞘板层结构致密;免疫荧光结果显示,MK-801组较Blank组成熟OLs(CC-1+/Olig2+)数量减少,MK-801+THIP组较MK-801组成熟OLs(CC-1+/Olig2+)数量增多(P均<0.05);Western blot结果显示,MK-801组较Blank组GPR17表达升高,MK-801+THIP组较MK-801组GPR17表达降低(P均<0.01)。结论 THIP可改善MK-801诱导的脑损伤模型小鼠学习记忆功能及髓鞘损伤程度,可能与其影响OLs分化有关。

天冬氨酸-谷氨酸载体1调节脑室周围白质软化早产鼠的髓鞘形成

背景:脑室周围白质软化是早产儿最严重的医疗并发症之一,目前尚无有效治疗措施。目的:探讨天冬氨酸-谷氨酸载体1(aspartate-glutamate carrier 1,AGC1)对脑室周围白质软化早产鼠髓鞘形成的调节作用。方法:60只出生后第2天雄性SD幼鼠随机分为假手术组和脑室周围白质软化组(n=30)。体外分离5只2日龄SD大鼠室周白质组织,制备白质祖细胞,建立实验性缺氧葡萄糖剥夺模型。分别在建立脑室周围白质软化、缺氧葡萄糖剥夺模型前,采用AGC1质粒(pcDNA3-AGC1)处理大鼠或细胞。在造模后不同时间点通过实时荧光定量PCR检测室周白质组织和细胞中AGC1表达。在脑室周围白质软化后14 d,采用免疫荧光法检测髓鞘碱性蛋白、别藻蓝蛋白表达,电子显微图像观察放射冠和胼胝体的超微结构。结果与结论:(1)在脑室周围白质软化后14 d,与假手术组相比,脑室周围白质软化组大鼠白质中髓鞘碱性蛋白表达、别藻蓝蛋白阳性少突胶质细胞数量以及有髓轴突数量显著减少(P<0.01);(2)与0 h相比,体内脑室周围白质软化开始后12-24 h时AGC1 mRNA表达显著升高(P<0.05),而在72 h-14 d时显著降低(P<0.05);(3)在体外对照条件下,与对照组相比,在缺氧葡萄糖剥夺后24-48 h时AGC1 mRNA表达显著升高(P<0.05),而在缺氧葡萄糖剥夺后7-14 d时AGC1 mRNA表达以及髓鞘碱性蛋白^(+)/AGC1^(+)少突胶质细胞形成显著降低(P<0.05);(4)pcDNA3-AGC1处理组在脑室周围白质软化后14 d处髓鞘碱性蛋白染色、别藻蓝蛋白阳性少突胶质细胞数量和有髓轴突数量比pcDNA3-NC对照组显著增多(P<0.05);(5)在体外实验中,增强AGC1表达进一步促进了缺氧葡萄糖剥夺后72h、7 d和14 d时少突胶质细胞前体细胞分化为髓鞘碱性蛋白^(+)/AGC1^(+)少突胶质细胞(P<0.05);提示脑室周围白质软化早产鼠模型和体外缺氧葡萄糖剥夺细胞模型中AGC1表达下调,通过上调AGC1可促进少突胶质细胞分化和髓鞘形成。

少突胶质前体细胞移植治疗脊髓损伤的研究进展

中枢神经系统(central nervous system,CNS)中的髓鞘在传递信息、营养神经元、维护内环境稳态等生物学过程中具有重要作用。脊髓损伤(spinal cord injury,SCI)造成的脱髓鞘极大限制了SCI后神经环路的重建和功能恢复。移植的外源性少突胶质前体细胞(oligodendrocyte progenitor cell,OPC)可以通过增殖、迁移、分化形成新的成熟髓鞘包裹轴突,弥补SCI后内源性髓鞘再生不足的缺陷,从而有效促进SCI后的神经修复。近年的研究已证明OPC移植治疗SCI的可行性,揭示了其促进感觉、运动功能恢复的机制。本文就当前OPC移植治疗SCI的研究进展进行综述,分析可能的治疗机制和潜在的组合疗法并进行展望,为基于移植OPC促进髓鞘再生治疗SCI修复提出新的策略和方向。