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| 1 | The contribution of oligodendrocytes and oligodendrocyte progenitor cells to central nervous system repair in multiple sclerosis: perspectives for remyelination therapeutic strategies显示文摘Oligodencrocytes(OLs) are the main glial cells of the central nervous system involved in myelination of axons. In multiple sclerosis(MS), there is an imbalance between demyelination and remyelination processes, the last one performed by oligodendrocyte progenitor cells(OPCs) and OLs, resulting into a permanent demyelination, axonal damage and neuronal loss. In MS lesions, astrocytes and microglias play an important part in permeabilization of blood-brain barrier and initiation of OPCs proliferation. Migration and differentiation of OPCs are influenced by various factors and the process is finalized by insufficient acummulation of OLs into the MS lesion. In relation to all these processes, the author will discuss the potential targets for remyelination strategies. | Adriana Octaviana Dulamea | 2017 | Neural Regeneration Research2017，12，12： | 9 |
| 2 | Epidural Spinal Cord Stimulation Promotes Motor Functional Recovery by Enhancing Oligodendrocyte Survival and Differentiation and by Protecting Myelin after Spinal Cord Injury in Rats显示文摘Epidural spinal cord stimulation (ESCS) markedly improves motor and sensory function after spinal cord injury (SCI), but the underlying mechanisms are unclear.Here, we investigated whether ESCS affects oligodendrocyte differentiation and its cellular and molecular mechanisms in rats with SCI. ESCS improved hindlimb motor function at 7 days, 14 days, 21 days, and 28 days after SCI.ESCS also significantly increased the myelinated area at 28days, and reduced the number of apoptotic cells in the spinal white matter at 7 days. SCI decreased the expression of 20,30-cyclic-nucleotide 30-phosphodiesterase (CNPase,an oligodendrocyte marker) at 7 days and that of myelin basic protein at 28 days. ESCS significantly upregulated these markers and increased the percentage of Sox2/CNPase/DAPI-positive cells (newly differentiated oligodendrocytes) at 7 days. Recombinant human bone morphogenetic protein 4 (rh BMP4) markedly downregulated these factors after ESCS. Furthermore, ESCS significantly decreased BMP4 and p-Smad1/5/9 expression after SCI,and rh BMP4 reduced this effect of ESCS. These findings indicate that ESCS enhances the survival and differentiation of oligodendrocytes, protects myelin, and promotes motor functional recovery by inhibiting the BMP4-Smad1/5/9 signaling pathway after SCI. | Gang Li Zhong-Kai Fan Guang-Fei Gu Zhi-Qiang Jia Qiang-Qiang Zhang Jun-Yu Dai Shi-Sheng He | 2020 | Neuroscience Bulletin2020，36，4： | 8 |
| 3 | Donepezil,a drug for Alzheimer’s disease,promotes oligodendrocyte generation and remyelination显示文摘Myelin sheaths play important roles in neuronal functions.In the central nervous system(CNS),the myelin is formed by oligodendrocytes(OLs),which are differentiated from oligodendrocyte precursor cells(OPCs).In CNS demyelinating disorders such as multiple sclerosis(MS),the myelin sheaths are damaged and the remyelination process is hindered.Small molecule drugs that promote OPC to OL differentiation and remyelination may provide a new way to treat these demyelinating diseases.Here we report that donepezil,an acetylcholinesterase inhibitor(AChEI)developed for the treatment of Alzheimer's disease(AD);significantly promotes OPC to OL differentiation.Interestingly,other AChEls,including huperzine A,rivastigmine,and tacrine,have no such effect indicating that donepezil's effect in promoting OPC differentiation is not dependent on the inhibition of AChE.Donepezil also facilitates the formation of myelin sheaths in OPC-DRG neuron co-culture.More interestingly,donepezil also promotes the repair of the myelin sheaths in vivo and provides significant therapeutic effect in a cuprizone-mediated demyelination animal model.Donepezil is a drug that has been used to treat AD safely for many years;our findings suggest that it might be repurposed to treat CNS demyelinating diseases such as MS by promoting OPC to OL differentiation and remyelination. | Xue Cui Yu-e Guo Jia-hui Fang Chang-jie Shi Na Suo Ru Zhang Xin Xie | 2019 | Acta Pharmacologica Sinica2019，40，11： | 7 |
| 4 | C-C chemokine receptor type 2-overexpressing exosomes alleviated experimental post-stroke cognitive impairment by enhancing microglia/macrophage M2 polarization显示文摘BACKGROUND Human-derived mesenchymal stromal cells have been shown to improve cognitive function following experimental stroke.The activity of exosomes has been verified to be comparable to the therapeutic effects of mesenchymal stromal cells.However,the effects of exosomes derived from human umbilical cord mesenchymal stem cells(HUC-MSCs)(ExoCtrl)on post-stroke cognitive impairment(PSCI)have rarely been reported.Moreover,whether exosomes derived from C-C chemokine receptor type 2(CCR2)-overexpressing HUC-MSCs(ExoCCR2)can enhance the therapeutic effects on PSCI and the possible underlying mechanisms have not been studied.AIM To investigate the effects of ExoCtrl on PSCI and whether ExoCCR2 can enhance therapeutic effects on PSCI.METHODS Transmission electron microscopy,qNano®particles analyzer,and Western blotting were employed to determine the morphology and CCR2 expression of ExoCtrl or ExoCCR2.ELISA was used to study the binding capacity of exosomes to CC chemokine ligand 2(CCL2)in vivo.After the intravenous injection of ExoCtrl or ExoCCR2 into experimental rats,the effect of ExoCtrl and ExoCCR2 on PSCI was assessed by Morris water maze.Remyelination and oligodendrogenesis were analyzed by Western blotting and immunofluorescence microscopy.QRT-PCR and immunofluorescence microscopy were conducted to compare the microglia/macrophage polarization.The infiltration and activation of hematogenous macrophages were analyzed by Western blotting and transwell migration analysis.RESULTS CCR2-overexpressing HUC-MSCs loaded the CCR2 receptor into their exosomes.The morphology and diameter distribution between ExoCtrl and ExoCCR2 showed no significant difference.ExoCCR2 bound significantly to CCL2 but ExoCtrl showed little CCL2 binding.Although both ExoCCR2 and ExoCtrl showed beneficial effects on PSCI,oligodendrogenesis,remyelination,and microglia/macrophage polarization,ExoCCR2 exhibited a significantly superior beneficial effect.We also found that ExoCCR2 could suppress the CCL2-induced macrophage migration and activation in vivo and in vitro,compared with ExoCtrl treated group.CONCLUSION CCR2 over-expression enhanced the therapeutic effects of exosomes on the experimental PSCI by promoting M2 microglia/macrophage polarization,enhancing oligodendrogenesis and remyelination.These therapeutic effects are likely through suppressing the CCL2-induced hematogenous macrophage migration and activation.Key words:Cognitive impairment;Stroke;Exosomes;C-C chemokine receptor type 2;Microglia/macrophage polarization;Remyelination. | Huai-Chun Yang Min Zhang Rui Wu Hai-Qing Zheng Li-Ying Zhang Jing Luo Li-Li Li Xi-Quan Hu | 2020 | World Journal of Stem Cells2020，12，2： | 6 |
| 5 | Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates Remyelination in Mice显示文摘The obstacle to successful remyelination in demyelinating diseases, such as multiple sclerosis, mainly lies in the inability of oligodendrocyte precursor cells(OPCs) to differentiate, since OPCs and oligodendrocytelineage cells that are unable to fully differentiate are found in the areas of demyelination. Thus, promoting the differentiation of OPCs is vital for the treatment of demyelinating diseases. Shikimic acid(SA) is mainly derived from star anise, and is reported to have antiinfluenza, anti-oxidation, and anti-tumor effects. In the present study, we found that SA significantly promoted the differentiation of cultured rat OPCs without affecting their proliferation and apoptosis. In mice, SA exerted therapeutic effects on experimental autoimmune encephalomyelitis(EAE), such as alleviating clinical EAE scores, inhibiting inflammation, and reducing demyelination in the CNS. SA also promoted the differentiation of OPCs as well as their remyelination after lysolecithin-induced demyelination.Furthermore, we showed that the promotion effect of SA on OPC differentiation was associated with the up-regulation of phosphorylated m TOR. Taken together, our resultsdemonstrated that SA could act as a potential drug candidate for the treatment of demyelinating diseases. | Fengfeng Lu Dou Yin Yingyan Pu Weili Liu Zhenghao Li Qi Shao Cheng He Li Cao | 2019 | Neuroscience Bulletin2019，35，3： | 4 |
| 6 | Decellularized optic nerve functional scaffold transplant facilitates directional axon regeneration and remyelination in the injured white matter of the rat spinal cord显示文摘Axon regeneration and remyelination of the damaged region is the most common repair strategy for spinal cord injury.However,achieving good outcome remains difficult.Our previous study showed that porcine decellularized optic nerve better mimics the extracellular matrix of the embryonic porcine optic nerve and promotes the directional growth of dorsal root ganglion neurites.However,it has not been reported whether this material promotes axonal regeneration in vivo.In the present study,a porcine decellularized optic nerve was seeded with neurotrophin-3-overexpressing Schwann cells.This functional scaffold promoted the directional growth and remyelination of regenerating axons.In vitro,the porcine decellularized optic nerve contained many straight,longitudinal channels with a uniform distribution,and microscopic pores were present in the channel wall.The spatial micro topological structure and extracellular matrix were conducive to the adhesion,survival and migration of neural stem cells.The scaffold promoted the directional growth of dorsal root ganglion neurites,and showed strong potential for myelin regeneration.Furthermore,we transplanted the porcine decellularized optic nerve containing neurotrophin-3-overexpressing Schwann cells in a rat model of T10 spinal cord defect in vivo.Four weeks later,the regenerating axons grew straight,the myelin sheath in the injured/transplanted area recovered its structure,and simultaneously,the number of inflammatory cells and the expression of chondroitin sulfate proteoglycans were reduced.Together,these findings suggest that porcine decellularized optic nerve loaded with Schwann cells overexpressing neurotrophin-3 promotes the directional growth of regenerating spinal cord axons as well as myelin regeneration.All procedures involving animals were conducted in accordance with the ethical standards of the Institutional Animal Care and Use Committee of Sun Yat-sen University(approval No.SYSU-IACUC-2019-B034)on February 28,2019. | Yu-Rong Bai Bi-Qin Lai Wei-Tao Han Jia-Hui Sun Ge Li Ying Ding Xiang Zeng Yuan-Huan Ma Yuan-Shan Zeng | 2021 | Neural Regeneration Research2021，16，11： | 4 |
| 7 | Heterogeneous populations of neural stem cells contribute to myelin repair显示文摘As ingenious as nature's invention of myelin sheaths within the mammalian nervous system is, as fatal can be damage to this specialized lipid structure. Long-term loss of electrical insulation and of further supportive functions myelin provides to axons, as seen in demyelinating diseases such as multiple sclerosis(MS), leads to neurodegeneration and results in progressive disabilities. Multiple lines of evidence have demonstrated the increasing inability of oligodendrocyte precursor cells(OPCs) to replace lost oligodendrocytes(OLs) in order to restore lost myelin. Much research has been dedicated to reveal potential reasons for this regeneration deficit but despite promising approaches no remyelination-promoting drugs have successfully been developed yet. In addition to OPCs neural stem cells of the adult central nervous system also hold a high potential to generate myelinating OLs. There are at least two neural stem cell niches in the brain, the subventricular zone lining the lateral ventricles and the subgranular zone of the dentate gyrus, and an additional source of neural stem cells has been located in the central canal of the spinal cord. While a substantial body of literature has described their neurogenic capacity, still little is known about the oligodendrogenic potential of these cells, even if some animal studies have provided proof of their contribution to remyelination. In this review, we summarize and discuss these studies, taking into account the different niches, the heterogeneity within and between stem cell niches and present current strategies of how to promote stem cell-mediated myelin repair. | Rainer Akkermann Felix Beyer Patrick Küry | 2017 | Neural Regeneration Research2017，12，4： | 3 |
| 8 | Induced pluripotent stem cell technology for spinal cord injury: a promising alternative therapy显示文摘Spinal cord injury has long been a prominent challenge in the trauma repair process. Spinal cord injury is a research hotspot by virtue of its difficulty to treat and its escalating morbidity. Furthermore, spinal cord injury has a long period of disease progression and leads to complications that exert a lot of mental and economic pressure on patients. There are currently a large number of therapeutic strategies for treating spinal cord injury, which range from pharmacological and surgical methods to cell therapy and rehabilitation training. All of these strategies have positive effects in the course of spinal cord injury treatment. This review mainly discusses the problems regarding stem cell therapy for spinal cord injury, including the characteristics and action modes of all relevant cell types. Induced pluripotent stem cells, which represent a special kind of stem cell population, have gained impetus in cell therapy development because of a range of advantages. Induced pluripotent stem cells can be developed into the precursor cells of each neural cell type at the site of spinal cord injury, and have great potential for application in spinal cord injury therapy. | Yu Li Ping-Ping Shen Bin Wang | 2021 | Neural Regeneration Research2021，16，8： | 3 |
| 9 | Rosmarinic acid ameliorates hypoxia/ischemia induced cognitive deficits and promotes remyelination显示文摘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. | Man Li Miao-Miao Cui Nwobodo Alexander Kenechukwu Yi-Wei Gu Yu-Lin Chen Si-Jing Zhong Yu-Ting Gao Xue-Yan Cao Li Wang Fu-Min Liu Xiang-Ru Wen | 2020 | Neural Regeneration Research2020，15，5： | 3 |
| 10 | Bone marrow mesenchymal stem cells and exercise restore motor function following spinal cord injury by activating PI3K/AKT/mTOR pathway显示文摘Although many therapeutic interventions have shown promise in treating spinal cord injury, focusing on a single aspect of repair cannot achieve successful and functional regeneration in patients following spinal cord injury. In this study, we applied a combinatorial approach for treating spinal cord injury involving neuroprotection and rehabilitation, exploiting cell transplantation and functional sensorimotor training to promote nerve regeneration and functional recovery. Here, we used a mouse model of thoracic contusive spinal cord injury to investigate whether the combination of bone marrow mesenchymal stem cell transplantation and exercise training has a synergistic effect on functional restoration. Locomotor function was evaluated by the Basso Mouse Scale, horizontal ladder test, and footprint analysis. Magnetic resonance imaging, histological examination, transmission electron microscopy observation, immunofluorescence staining, and western blotting were performed 8 weeks after spinal cord injury to further explore the potential mechanism behind the synergistic repair effect. In vivo, the combination of bone marrow mesenchymal stem cell transplantation and exercise showed a better therapeutic effect on motor function than the single treatments. Further investigations revealed that the combination of bone marrow mesenchymal stem cell transplantation and exercise markedly reduced fibrotic scar tissue, protected neurons, and promoted axon and myelin protection. Additionally, the synergistic effects of bone marrow mesenchymal stem cell transplantation and exercise on spinal cord injury recovery occurred via the PI3 K/AKT/mTOR pathway. In vitro, experimental evidence from the PC12 cell line and primary cortical neuron culture also demonstrated that blocking of the PI3 K/AKT/mTOR pathway would aggravate neuronal damage. Thus, bone marrow mesenchymal stem cell transplantation combined with exercise training can effectively restore motor function after spinal cord injury by activating the PI3 K/AKT/mTOR pathway. | Xin Sun Li-Yi Huang Hong-Xia Pan Li-Juan Li Lu Wang Gai-Qin Pei Yang Wang Qing Zhang Hong-Xin Cheng Cheng-Qi He Quan Wei | 2023 | Neural Regeneration Research2023，18，5： | 3 |
| 11 | Activation of TRPV1 receptor facilitates myelin repair following demyelination via the regulation of microglial function显示文摘The transient receptor potential vanilloid 1(TRPV1)is a non-selective cation channel that is activated by capsaicin(CAP),the main component of chili pepper.Despite studies in several neurological diseases,the role of TRPV1 in demyelinating diseases remains unknown.Herein,we reported that TRPV1 expression was increased within the corpus callosum during demyelination in a cuprizone(CPZ)-induced demyelination mouse model.TRPV1 deficiency exacerbated motor coordinative dysfunction and demyelination in CPZ-treated mice,whereas the TRPV1 agonist CAP improved the behavioral performance and facilitated remyelination.TRPV1 was predominantly expressed in Iba1+microglia/macrophages in human brain sections of multiple sclerosis patients and mouse corpus callosum under demyelinating conditions.TRPV1 deficiency decreased microglial recruitment to the corpus callosum,with an associated increase in the accumulation of myelin debris.Conversely,the activation of TRPV1 by CAP enhanced the recruitment of microglia to the corpus callosum and potentiated myelin debris clearance.Using real-time live imaging we confirmed an increased phagocytic function of microglia following CAP treatment.In addition,the expression of the scavenger receptor CD36 was increased,and that of the glycolysis regulators Hif1a and Hk2 was decreased.We conclude that TRPV1 is an important regulator of microglial function in the context of demyelination and may serve as a promising therapeutic target for demyelinating diseases such as multiple sclerosis. | Jing-xian Sun Ke-ying Zhu Yu-meng Wang Dan-jie Wang Mi-zhen Zhang Heela Sarlus Irene Benito-Cuesta Xiao-qiang Zhao Zao-feng Zou Qing-yang Zhong Yi Feng Shuai Wu Yan-qing Wang Robert A.Harris Jun Wang | 2023 | Acta Pharmacologica Sinica2023，44，4： | 2 |
| 12 | Intravenous transplantation of mouse embryonic stem cells attenuates demyelination in an ICR outbred mouse model of demyelinating diseases显示文摘Induction of demyelination in the central nervous system(CNS) of experimental mice using cuprizone is widely used as an animal model for studying the pathogenesis and treatment of demyelination. However, different mouse strains used result in different pathological outcomes. Moreover, because current medicinal treatments are not always effective in multiple sclerosis patients, so the study of exogenous cell transplantation in an animal model is of great importance. The aims of the present study were to establish an alternative ICR outbred mouse model for studying demyelination and to evaluate the effects of intravenous cell transplantation in the present developed mouse model. Two sets of experiments were conducted. Firstly, ICR outbred and BALB/c inbred mice were fed with 0.2% cuprizone for 6 consecutive weeks; then demyelinating scores determined by luxol fast blue stain or immunolabeling with CNPase were evaluated. Secondly, attenuation of demyelination in ICR mice by intravenous injection of m ES cells was studied. Scores for demyelination in the brains of ICR mice receiving cell injection(m ES cells-injected group) and vehicle(sham-inoculated group) were assessed and compared. The results showed that cuprizone significantly induced demyelination in the cerebral cortex and corpus callosum of both ICR and BALB/c mice. Additionally, intravenous transplantation of m ES cells potentially attenuated demyelination in ICR mice compared with sham-inoculated groups. The present study is among the earliest reports to describe the cuprizone-induced demyelination in ICR outbred mice. Although it remains unclear whether m ES cells or trophic effects from m ES cells are the cause of enhanced remyelination, the results of the present study may shed some light on exogenous cell therapy in central nervous system demyelinating diseases. | Kidsadagon Pringproa Anucha Sathanawongs Chananthida Khamphilai Sarocha Sukkarinprom Apichart Oranratnachai | 2016 | Neural Regeneration Research2016，11，10： | 2 |
| 13 | Dynamic glial response and crosstalk in demyelination-remyelination and neurodegeneration processes显示文摘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. | Tianci Chu Lisa B.E.Shields Wenxin Zeng Yi Ping Zhang Yuanyi Wang Gregory N.Barnes Christopher B.Shields Jun Cai | 2021 | Neural Regeneration Research2021，16，7： | 2 |
| 14 | Poly-L-ornithine blocks the inhibitory effects of fibronectin on oligodendrocyte differentiation and promotes myelin repair显示文摘The extracellular matrix surrounding oligodendrocytes plays an important role during myelination and remyelination in the brain.In many cases,the microenvironment surrounding demyelination lesions contains inhibitory molecules,which lead to repair failure.Accordingly,blocking the activity of these inhibitory factors in the extracellular matrix should lead to more successful remyelination.In the central nervous system,oligodendrocytes form the myelin sheath.We performed primary cell culture and found that a natural increase in fibronectin promoted the proliferation of oligodendrocyte progenitors during the initial stage of remyelination while inhibiting oligodendrocyte differentiation.Poly-L-ornithine blocked these inhibitory effects without compromising fibronectin’s pro-proliferation function.Experiments showed that poly-L-ornithine activated the Erk1/2 signaling pathway that is necessary in the early stages of differentiation,as well as PI3K signaling pathways that are needed in the mid-late stages.When poly-L-ornithine was tested in a lysolecithin-induced animal model of focal demyelination,it enhanced myelin regeneration and promoted motor function recovery.These findings suggest that poly-L-ornithine has the potential to be a treatment option for clinical myelin sheath injury. | Ya-Jie Xiong Shahid Hussain Soomro Zhong-Hai Huang Pan-Pan Yu Jie Ping Hui Fu | 2023 | Neural Regeneration Research2023，18，4： | 1 |
| 15 | Oligodendrocyte precursor cell maturation: role of adenosine receptors显示文摘Oligodendrocyte-formed myelin sheaths allow fast synaptic transmission in the brain and their degeneration leads to demyelinating diseases such as multiple sclerosis. Remyelination requires the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes but, in chronic neurodegenerative disorders, remyelination fails due to adverse environment. Therefore, a strategy to prompt oligodendrocyte progenitor cell differentiation towards myelinating oligodendrocytes is required. The neuromodulator adenosine, and its receptors(A1, A(2A), A(2B) and A3 receptors: A1R, A(2A)R, A(2B)R and A3R), are crucial mediators in remyelination processes. It is known that A1Rs facilitate oligodendrocyte progenitor cell maturation and migration whereas the A3Rs initiates apoptosis in oligodendrocyte progenitor cells. Our group of research contributed to the field by demonstrating that A(2A)R and A(2B)R inhibit oligodendrocyte progenitor cell maturation by reducing voltage-dependent K^+ currents necessary for cell differentiation. The present review summarizes the possible role of adenosine receptor ligands as potential therapeutic targets in demyelinating pathologies such as multiple sclerosis. | Federica Cherchi Anna Maria Pugliese Elisabetta Coppi | 2021 | Neural Regeneration Research2021，16，9： | 1 |
| 16 | Acupuncture effects on serum myelin basic protein and remyelination following 30 minutes and 2 hours of ischemia in a rat model of cerebral ischemia-reperfusion injury显示文摘BACKGROUND:Acupuncture treatment on injured cerebral axons has shown to provide efficacy in clinical practice.It is unknown whether acupuncture produces therapeutic effects by protecting injured cerebral myelin in ischemic stroke.OBJECTIVE:To test whether acupuncture provides protection for injured cerebral myelin,based on quantitative data from cerebral ischemia-reperfusion rats,and to compare the effects of early and late acupuncture on serum myelin basic protein(MBP) content and remyelination of the ischemic internal capsule.DESIGN,TIME AND SETTING:A randomized,controlled experiment was performed at the Neuro-biological Laboratory,Sichuan University from March 2005 to March 2006.MATERIALS:'Hua Tuo' Brand filiform needles were produced by the Medical Instrument Factory of Suzhou,China.METHODS:A total of 52 adult,healthy,male,Sprague Dawley rats were randomly assigned to four groups:control(n=4),model(n=16),early acupuncture(n=16),and late acupuncture(n=16).The focal cerebral ischemia-reperfusion model was established by middle cerebral artery occlusion in the right hemisphere using the modified thread embolism method in the latter three groups.Early and late acupuncture groups underwent acupuncture after ischemia for 30 minutes and 2 hours using the Xingnaokaiqiao needling method,respectively.Acupoints were 'Neiguan'(PC 6) and 'Sanyinjiao'(SP 6) on the bilateral sides,as well as 'Shuigou'(DU 26) and 'Baihui'(DU 20) with stimulation for 1 minute at each acupoint.Acupuncture at all acupoints was performed two or three times while the needle was retained,once per day.No special handling was administered to the control group.MAIN OUTCOME MEASURES:For each group,remyelination of the internal capsule was observed by Pal-Weigert's myelin staining and serum MBP content was detected using enzyme-linked immunosorbent assay method on days 1,3,5,and 7 following ischemia-reperfusion injury.RESULTS:Compared with the control group,massive demyelination of the internal capsule occurred,and serum MBP content increased in the model group(P<0.05).Compared with the model group,the extent of demyelination in the internal capsule was less distinct and serum MBP content was significantly less in the early and late acupuncture group(P<0.01).Compared with the late acupuncture group,serum MBP content reached a peak later and the peak value was less in the early acupuncture group.CONCLUSION:Results suggest that acupuncture exerts a protective effect on injured cerebral myelin in ischemia-reperfusion rats by reducing serum MBP content and promoting remyelination.The study also suggests that the effect of early acupuncture is superior to late acupuncture. | Jiangang Duan Ming Liu | 2010 | Neural Regeneration Research2010，5，4： | 1 |
| 17 | Progesterone effects on the oligodendrocyte linage: all roads lead to the progesterone receptor显示文摘A new role has emerged for progesterone after discovering its potent actions away from reproduction in both the central and the peripheral nervous system. The aim of the present report is to discuss progesterone’s mechanisms of action involved in myelination, remyelination and neuroinflammation. The pivotal role of the classic progesterone receptor is described and evidence is compiled about progesterone’s direct effects on oligodendrocyte linage and its indirect effects on oligodendrocyte precursor cell differentiation by decreasing the neuroinflammatory environment. | Ignacio Jure Alejandro F. De Nicola Florencia Labombarda | 2019 | Neural Regeneration Research2019，14，12： | 1 |
| 18 | Pinocembrin Promotes OPC Differentiation and Remyelination via the mTOR Signaling Pathway显示文摘The exacerbation of progressive multiple sclerosis(MS)is closely associated with obstruction of the differentiation of oligodendrocyte progenitor cells(OPCs).To discover novel therapeutic compounds for enhancing remyelination by endogenous OPCs,we screened for myelin basic protein expression using cultured rat OPCs and a library of small-molecule compounds.One of the most effective drugs was pinocembrin,which remarkably promoted OPC differentiation and maturation without affecting cell proliferation and survival.Based on these in vitro effects,we further assessed the therapeutic effects of pinocembrin in animal models of demyelinating diseases.We demonstrated that pinocembrin significantly ameliorated the progression of experimental autoimmune encephalomyelitis(EAE)and enhanced the repair of demyelination in lysolectin-induced lesions.Further studies indicated that pinocembrin increased the phosphorylation level of mammalian target of rapamycin(mTOR).Taken together,our results demonstrated that pinocembrin promotes OPC differentiation and remyelination through the phosphorylated mTOR pathway,and suggest a novel therapeutic prospect for this natural flavonoid product in treating demyelinating diseases. | Qi Shao Ming Zhao Wenwen Pei Yingyan Pu Mingdong Liu Weili Liu Zhongwang Yu Kefu Chen Hong Liu Benqiang Deng Li Cao | 2021 | Neuroscience Bulletin2021，37，9： | 1 |
| 19 | Neuronal gene transcription modulates demyelination and remyelination in a mouse model of multiple sclerosis显示文摘The role of the neuronal compartment in multiple sclerosis:Multiple sclerosis(MS)is a chronic inflammatory demyelinating disease affecting the central nervous system(CNS).It is usually characterized by initial relapses and remissions with subsequent progressive neurological deterioration.MS is the most common acquired neurological disorder affecting | Sofia Anastasiadou Bernd Knoll | 2015 | Neural Regeneration Research2015，10，9： | 0 |
| 20 | In vivo imaging reveals mature Oligodendrocyte division in adult Zebrafish显示文摘Whether mature oligodendrocytes(mOLs)participate in remyelination has been disputed for several decades.Recently,some studies have shown that mOLs participate in remyelination by producing new sheaths.However,whether mOLs can produce new oligodendrocytes by asymmetric division has not been proven.Zebrafish is a perfect model to research remyelination compared to other species.In this study,optic nerve crushing did not induce local mOLs death.After optic nerve transplantation from olig2:eGFP fish to AB/WT fish,olig2^(+)cells from the donor settled and rewrapped axons in the recipient.After identifying these rewrapping olig2^(+)cells as mOLs at 3 months posttransplantation,in vivo imaging showed that olig2^(+)cells proliferated.Additionally,in vivo imaging of new olig2^(+)cell division from mOLs was also captured within the retina.Finally,fine visual function was renewed after the remyelination program was completed.In conclusion,our in vivo imaging results showed that new olig2^(+)cells were born from mOLs by asymmetric division in adult zebrafish,which highlights the role of mOLs in the progression of remyelination in the mammalian CNS. | Suqi Zou Bing Hu | 2021 | Cell Regeneration2021，10，1： | 0 |
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