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Neuroscience Bulletin 2024年第3期40卷 283-292页

作者： Yunyi Lan Xinyan Han Fei Huang Hailian Shi Hui Wu Liu Yang Zhibi Hu Xiaojun Wu Shanghai Key Laboratory of Compound Chinese Medicines The Ministry of Education Key Laboratory for Standardization of Chinese MedicinesThe State Administration of TCM Key Laboratory for New Resources and Quality Evaluation of Chinese MedicineInstitute of Chinese Materia MedicaShanghai University of Traditional Chinese MedicineShanghai201203China Central Laboratory Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai200021China

Early growth response protein 1(Egr-1)triggers the transcription of many genes involved in cell growth,differentiation,synaptic plasticity,and neurogenesis.However,its mechanism in neuronal survival and degeneration is still poorly understood.This study demonstrated that Egr-1 was down-regulated at mRNA and protein levels in the central nervous system(CNS)of Experimental autoimmune encephalomyelitis(EAE)mice.Egr-1 knockout exacerbated EAE progression in mice,as shown by increased disease severity and incidence;it also aggravated neuronal apoptosis,which was associated with weakened activation of the BDNF/TGFβ1/MAPK/Akt signaling pathways in the CNS of EAE mice.Consistently,Egr-1 siRNA promoted apoptosis but mitigated the activation of BDNF/TGFβ1/MAPK/Akt signaling in SH-SY5Y cells.Our results revealed that Egr-1 is a crucial regulator of neuronal survival in EAE by regulating TGFβ1-mediated signaling activation,implicating the important role of Egr-1 in the pathogenesis of multiple sclerosis as a potential novel therapy target.

关键词： Early growth response protein 1 Transforming growth factor-beta 1 Multiple sclerosis Experimental autoimmune encephalomyelitis Neurodegeneration

Emodin attenuates inflammation and demyelination in Experimental autoimmune encephalomyelitis

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Neural Regeneration Research 2023年第7期18卷 1535-1541页

作者： Yue-Ran Cui Zhong-Qi Bu Hai-Yang Yu Li-Li Yan Juan Feng Department of Neurology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous system.However,the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown.In this study,a rat model of Experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis,and the rats were intraperitoneally injected with emodin(20 mg/kg/d)from the day of immune induction until they were sacrificed.In this model,the nucleotide-binding domain-like receptor family pyrin domain containing 3(NLRP3)inflammasome and the microglia exacerbated neuroinflammation,playing an important role in the development of multiple sclerosis.In addition,silent information regulator of transcription 1(SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator(PGC-1α)was found to inhibit activation of the NLRP3 inflammasome,and SIRT1 activation reduced disease severity in Experimental autoimmune encephalomyelitis.Furthermore,treatment with emodin decreased body weight loss and neurobehavioral deficits,alleviated inflammatory cell infiltration and demyelination,reduced the expression of inflammatory cytokines,inhibited microglial aggregation and activation,decreased the levels of NLRP3 signaling pathway molecules,and increased the expression of SIRT1 and PGC-1α.These findings suggest that emodin improves the symptoms of Experimental autoimmune encephalomyelitis,possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation.These findings provide experimental evidence for treatment of multiple sclerosis with emodin,enlarging the scope of clinical application for emodin.

关键词： demyelination emodin Experimental autoimmune encephalomyelitis microglia multiple sclerosis neuroinflammation NLRP3 inflammasome PGC-1α pyroptosis SIRT1

Grape Seed Extract Attenuates Demyelination in Experimental autoimmune encephalomyelitis Mice by Inhibiting Inflammatory Response of Immune Cells

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Chinese Journal of Integrative Medicine 2023年第5期29卷 394-404页

作者： WANG Qing CHEN Yang-yang YANG Zhi-chao YUAN Hai-jun DONG Yi-wei MIAO Qiang LI Yan-qing WANG Jing YU Jie-zhong XIAO Bao-guo MA Cun-gen Research Center of Neurobiology the Key Research Laboratory of Benefiting Qi for Acting Blood Circulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese MedicineShanxi University of Chinese MedicineJinzhongShanxi Province(030619)China Department of Neurology the First Affiliated HospitalShanxi Medical UniversityTaiyuan(030001)China Institute of Brain Science Shanxi Key Laboratory of Inflammatory Neurodegenerative DiseasesShanxi Datong UniversityDatongShanxi Province(037009)China Department of Neurology Datong Fifth People's HospitalDatongShanxi Province(037009)China Institute of Neurology Huashan HospitalInstitutes of Brain Science and State Key Laboratory of Medical NeurobiologyFudan UniversityShanghai(200000)China

Objective: To examine the anti-inflammatory effect of grape seed extract(GSE) in animal and cellular models and explore its mechanism of action. Methods: This study determined the inhibitory effect of GSE on macrophage inflammation and Th1 and Th17 polarization in vitro. Based on the in vitro results, the effects and mechanisms of GSE on multiple sclerosis(MS)-Experimental autoimmune encephalomyelitis(EAE) mice model were further explored. The C57BL/6 mice were intragastrically administered with 50 mg/kg of GSE once a day from the 3rd day to the 27th day after immunization. The activation of microglia, the polarization of Th1 and Th17and the inflammatory factors such as tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-6, IL-12, IL-17and interferon-γ(IFN-γ) secreted by them were detected in vitro and in vivo by flow cytometry, enzyme linked immunosorbent assay(ELISA), immunofluorescence staining and Western blot, respectively. Results: GSE reduced the secretion of TNF-α, IL-1β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide(P<0.01), inhibited the secretion of TNF-α, IL-1β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days(P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors(P<0.01). GSE significantly improved the clinical symptoms of EAE mice, and inhibited spinal cord demyelination and inflammatory cell infiltration. Peripherally, GSE downregulated the expression of toll-like-receptor 4(TLR4) and Rho-associated kinase(ROCKⅡ, P<0.05 or P<0.01), and inhibited the secretion of inflammatory factors(P<0.01 or P<0.05). In the central nervous system, GSE inhibited the infiltration of CD45+CD11b+and CD45+CD4+cells, and weakened the differentiation of Th1 and Th17(P<0.05). Moreover, it reduced the secretion of inflammatory factors(P<0.01), and prevented the activation of microglia(P<0.05). Conclusion: GSE had a beneficial effect on the pathogenesis and progression of EAE by inhibiting inflammatory response as a

关键词： grape seed extract Experimental autoimmune encephalomyelitis demyelination inﬂammatory cell inﬂammatory factor

Targeting central nervous system extracellular vesicles enhanced triiodothyronine remyelination effect on Experimental autoimmune encephalomyelitis

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Bioactive Materials 2022年第3期7卷 373-384页

作者： Yun Xiao Jing Tian Wen-Cheng Wu Yu-Han Gao Yu-Xin Guo Sheng-Jiao Song Rui Gao Li-Bin Wang Xiao-Yu Wu Yuan Zhang Xing Li National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China The Key Laboratory of Medicinal Resources and Natural Pharmaceutical ChemistryThe Ministry of EducationCollege of Life SciencesShaanxi Normal UniversityXi’anShaanxi710119China The General Hospital of Ningxia Medical University Yinchuan750001China

The lack of targeted and high-efficiency drug delivery to the central nervous system(CNS)nidus is the main problem in the treatment of demyelinating disease.Extracellular vesicles(EVs)possess great promise as a drug delivery vector given their advanced features.However,clinical applications are limited because of their inadequate targeting ability and the“dilution effects”after systemic administration.Neural stem cells(NSCs)supply a plentiful source of EVs on account of their extraordinary capacity for self-renewal.Here,we have developed a novel therapeutic system using EVs from modified NSCs with high expressed ligand PDGF-A(EVPs)and achieve local delivery.It has been demonstrated that EVPs greatly enhance the target capability on oligodendrocyte lineage.Moreover,EVPs are used for embedding triiodothyronine(T3),a thyroid hormone that is critical for oligodendrocyte development but has serious side effects when systemically administered.Our results demonstrated that systemic injection of EVPs+T3,versus EVPs or T3 administration individually,markedly alleviated disease development,enhanced oligodendrocyte survival,inhibited myelin damage,and promoted myelin regeneration in the lesions of Experimental autoimmune encephalomyelitis mice.Taken together,our findings showed that engineered EVPs possess a remarkable CNS lesion targeting potential that offers a potent therapeutic strategy for CNS demyelinating diseases as well as neuroinflammation.

关键词： Extracellular vesicles Neuroinflammation Multiple sclerosis Drug delivery Experimental autoimmune encephalomyelitis T3

Cornuside alleviates Experimental autoimmune encephalomyelitis by inhibiting Th17 cell infiltration into the central nervous system

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2021年第5期22卷 421-430页

作者： Rongbo ZHANG Jin LIU Bin XU You WU Shunli LIANG Qiang YUAN Department of Neurology the Second Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310005China College of Pharmacy Zhejiang Chinese Medical UniversityHangzhou 310053China

The present study was conducted to clarify the therapeutic effect of cornuside on Experimental autoimmune encephalomyelitis(EAE)and its influence on T helper 17(Th17)cell and regulatory T(Treg)cell infiltration into the central nervous system.Rats were randomly placed into four treatment groups:control,EAE,EAE+cornuside,and EAE+prednisolone.The neurological function scores of rats were assessed daily.On the second day after EAE rats began to show neurological deficit symptoms,the four groups were treated with normal saline,normal saline,cornuside(150 mg/kg),and prednisolone(5 mg/kg),respectively.The treatment was discontinued after two weeks,and the spinal cord was obtained for hematoxylin and eosin(H&E)and luxol fast blue staining,as well as retinoic acid receptor-related orphan receptorγ(RORγ)and forkhead box protein P3(Foxp3)immunohistochemical staining.Blood was collected for Th17 and Treg cell flow cytometry testing,and the serum levels of interleukin(IL)-17A,IL-10,transforming growth factor-β(TGF-β),IL-6,IL-23,and IL-2 were measured via enzymelinked immunosorbent assay(ELISA).Compared with rats in the EAE group,rats in the EAE+cornuside and EAE+prednisolone groups began to recover from neurological deficits earlier,and had a greater degree of improvement of symptoms.Focal inflammation,demyelination,and RORγ-positive cell infiltration were reduced by cornuside or prednisolone treatment,whereas the Foxp3-positive cell numbers were not significantly different.Meanwhile,the number of Th17 cells and the IL-17A,IL-6,and IL-23 levels were lower in the blood after cornuside or prednisolone treatment,whereas the number of Treg cells or the levels of IL-10,TGF-β,and IL-2 were not markedly different.Cornuside can alleviate symptoms of EAE neurological deficits through its anti-inflammatory and immunosuppressive effects,and Th17 cells may be one of its therapeutic targets.

关键词： Cornuside Experimental autoimmune encephalomyelitis Multiple sclerosis Inflammation

MicroRNAs as disease progression biomarkers and therapeutic targets in Experimental autoimmune encephalomyelitis model of multiple sclerosis

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Neural Regeneration Research 2020年第10期15卷 1831-1837页

作者： Bridget Martinez Philip V.Peplow Physical Chemistry and Applied Spectroscopy Chemistry DivisionLos Alamos National LaboratoryLos AlamosNMUSA Department of Medicine St.Georges University School of MedicineGrenada Department of Anatomy University of OtagoDunedinNew Zealand

Multiple sclerosis is an autoimmune neurodegenerative disease of the central nervous system characterized by pronounced inflammatory infiltrates entering the brain,spinal cord and optic nerve leading to demyelination.Focal demyelination is associated with relapsing-remitting multiple sclerosis,while progressive forms of the disease show axonal degeneration and neuronal loss.The tests currently used in the clinical diagnosis and management of multiple sclerosis have limitations due to specificity and sensitivity.MicroRNAs(miRNAs)are dysregulated in many diseases and disorders including demyelinating and neuroinflammatory diseases.A review of recent studies with the Experimental autoimmune encephalomyelitis animal model(mostly female mice 6–12 weeks of age)has confirmed miRNAs as biomarkers of Experimental autoimmune encephalomyelitis disease and importantly at the pre-onset(asymptomatic)stage when assessed in blood plasma and urine exosomes,and spinal cord tissue.The expression of certain miRNAs was also dysregulated at the onset and peak of disease in blood plasma and urine exosomes,brain and spinal cord tissue,and at the post-peak(chronic)stage of Experimental autoimmune encephalomyelitis disease in spinal cord tissue.Therapies using miRNA mimics or inhibitors were found to delay the induction and alleviate the severity of Experimental autoimmune encephalomyelitis disease.Interestingly,Experimental autoimmune encephalomyelitis disease severity was reduced by overexpression of miR-146a,miR-23b,miR-497,miR-26a,and miR-20b,or by suppression of miR-182,miR-181c,miR-223,miR-155,and miR-873.Further studies are warranted on determining more fully miRNA profiles in blood plasma and urine exosomes of Experimental autoimmune encephalomyelitis animals since they could serve as biomarkers of asymptomatic multiple sclerosis and disease course.Additionally,studies should be performed with male mice of a similar age,and with aged male and female mice.

关键词： animal model blood plasma blood serum brain tissue disease biomarkers Experimental autoimmune encephalomyelitis microRNAs multiple sclerosis spinal cord therapeutic targets urine exosomes

MiR-125a-5p Regulates Vitamin D Receptor Expression in a Mouse Model of Experimental autoimmune encephalomyelitis

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Neuroscience Bulletin 2020年第2期36卷 110-120页

作者： Han-Chun Long Rui Wu Chun-Feng Liu Fei-Long Xiong Zu Xu Dian He Yi-Fan Zhang Bing Shao Ping-An Zhang Guang-Yin Xu Lan Chu Department of Neurology The Affiliated Hospital of Guizhou Medical UniversityGuiyang 550001China Department of Neurology The Second Affiliated Hospital of Soochow UniversitySuzhou 215008China Institute of Neuroscience Soochow UniversitySuzhou 215123China Department of Neurology The Affiliated Xingyi City Hospital of Guizhou Medical UniversityXingyi 562400China

Multiple sclerosis(MS)is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system.Although the symptoms of MS can be managed by vitamin D3 treatment alone,this condition cannot be completely eradicated.Thus,there might be unknown factors capable of regulating the vitamin D receptor(VDR).Genome-wide analysis showed that miRNAs were associated with VDRs.We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS,mice with Experimental autoimmune encephalomyelitis(EAE),which was induced by myelin oligodendrocyte glycoprotein 35–55 peptides.EAE mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control mice.And inflammatory infiltration was found in the lumbosacral spinal cord of EAE mice.In addition,VDR expression was significantly lower while the expression of miR-125a-5p was markedly higher in the spinal ventral horn of EAE mice than in vehicle or control mice.Importantly,activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE mice.Interestingly,VDR and miR-125a-5p were co-localized in the same neurons of the ventral horn.More importantly,inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE mice.These results support a critical role for miR-125a-5p in modulating VDR activity in EAE and suggest potential novel therapeutic interventions.

关键词： Multiple sclerosis Experimental autoimmune encephalomyelitis Vitamin D receptor MiR-125a-5p Myelin oligodendrocyte glycoprotein 35-55 peptides

Nogo receptor expression in microglia/macrophages during Experimental autoimmune encephalomyelitis progression

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Neural Regeneration Research 2018年第5期13卷 896-907页

作者： Amani A.Alrehaili Jae Young Lee Maha M.Bakhuraysah Min Joung Kim Pei-Mun Aui Kylie A.Magee Steven Petratos Department of Neuroscience Central Clinical School Monash University Department of Clinical Laboratories College of Applied Medical Sciences Taif University Toolgen Inc. Gasan Digital-Ro

Myelin-associated inhibitory factors within the central nervous system（CNS） are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1（NgR1） has been well documented to play a key role in limiting axonal regrowth in the injured and diseased mammalian CNS. However, the role of nogo receptor in immune cell activation during CNS inflammation is yet to be mechanistically elucidated. Microglia/macrophages are immune cells that are regarded as pathogenic contributors to inflammatory demyelinating lesions in multiple sclerosis（MS）. In this study, the animal model of MS, Experimental autoimmune encephalomyelitis（EAE） was induced in ngr1^＋/＋ and ngr1^–/– female mice following injection with the myelin oligodendrocyte glycoprotein（MOG_（35–55）） peptide. A fatemap analysis of microglia/macrophages was performed throughout spinal cord sections of EAE-induced mice at clinical scores of 0, 1, 2 and 3, respectively（increasing locomotor disability） from both genotypes, using the CD11 b and Iba1 cell markers. Western immunoblotting using lysates from isolated spinal cord microglia/macrophages, along with immunohistochemistry and flow cytometric analysis, was performed to demonstrate the expression of nogo receptor and its two homologs during EAE progression. Myelin protein engulfment during EAE progression in ngr1^＋/＋ and ngr1^–/– mice was demonstrated by western immunblotting of lysates from isolated spinal cord microglia/macrophages, detecting levels of Nogo-A and MOG. The numbers of M1 and M2 microglia/macrophage phenotypes present in the spinal cords of EAE-induced ngr1^＋/＋ and ngr1^–/– mice, were assessed by flow cytometric analysis using CD38 and Erg-2 markers. A significant difference in microglia/macrophage numbers between ngr1^＋/＋ and ngr1^–/– mice was identified during the progression of the clinical symptoms of EAE, in the white versus gray matter regions of the spinal cord. This difference was unrelated to the expression of Ng R on these macrophage/microglial

关键词： microglia Experimental autoimmune encephalomyelitis nogo receptor myelin-associated inhibitory factors （MAIFs） Nogo A neural regeneration

Role of nuclear factor κB in multiple sclerosis and Experimental autoimmune encephalomyelitis

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Neural Regeneration Research 2018年第9期13卷 1507-1515页

作者： Yuan Yue Sarrabeth Stone Wensheng Lin Department of Neuroscience University of Minnesota Institute for Translational Neuroscience University of Minnesota

The transcription factor nuclear factor κB（NF-κB） plays major roles in inflammatory diseases through regulation of inflammation and cell viability.Multiple sclerosis（MS） is a chronic inflammatory demyelinating and neurodegenerative disease of the central nervous system（CNS）.It has been shown that NF-κB is activated in multiple cell types in the CNS of MS patients,including T cells,microglia/macrophages,astrocytes,oligodendrocytes,and neurons.Interestingly,data from animal model studies,particularly studies of Experimental autoimmune encephalomyelitis,have suggested that NF-κB activation in these individual cell types has distinct effects on the development of MS.In this review,we will cover the current literature on NF-κB and the evidence for its role in the development of MS and its animal model Experimental autoimmune encephalomyelitis.

关键词： multiple sclerosis Experimental autoimmune encephalomyelitis nuclear-factor κB T cell macrophage microglia astrocyte oligodendrocyte neuron

Fasudil-modified macrophages reduce inflammation and regulate the immune response in Experimental autoimmune encephalomyelitis

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Neural Regeneration Research 2024年第3期19卷 671-679页

作者： Chunyun Liu Shangde Guo Rong Liu Minfang Guo Qing Wang Zhi Chai Baoguo Xiao Cungen Ma Institute of Brain Science Shanxi Datong UniversityDatongShanxi ProvinceChina The Key Research Laboratory of Benefiting Qi for Acting Blood Cireulation Method to Treat Multiple Sclerosis of State Administration of Traditional Chinese Medicine/Research Center of Neurobiology Shanxi University of Chinese MedicineTaiyuanShanxi ProvinceChina Institute of Neurology Huashan HospitalInstitutes of Brain Science and State Key Laboratory of Medical NeurobiologyFudan UniversityShanghaiChina

Multiple sclerosis is characterized by demyelination and neuronal loss caused by inflammatory cell activation and infiltration into the central nervous system.Macrophage polarization plays an important role in the pathogenesis of Experimental autoimmune encephalomyelitis,a traditional experimental model of multiple sclerosis.This study investigated the effect of Fasudil on macrophages and examined the therapeutic potential of Fasudil-modified macrophages in Experimental autoimmune encephalomyelitis.We found that Fasudil induced the conversion of macrophages from the pro-inflammatory M1 type to the anti-inflammatory M2 type,as shown by reduced expression of inducible nitric oxide synthase/nitric oxide,interleukin-12,and CD16/32 and increased expression of arginase-1,interleukin-10,CD14,and CD206,which was linked to inhibition of Rho kinase activity,decreased expression of toll-like receptors,nuclear factor-κB,and components of the mitogen-activated protein kinase signaling pathway,and generation of the pro-inflammatory cytokines tumor necrosis factor-α,interleukin-1β,and interleukin-6.Crucially,Fasudil-modified macrophages effectively decreased the impact of Experimental autoimmune encephalomyelitis,resulting in later onset of disease,lower symptom scores,less weight loss,and reduced demyelination compared with unmodified macrophages.In addition,Fasudil-modified macrophages decreased interleukin-17 expression on CD4^(+)T cells and CD16/32,inducible nitric oxide synthase,and interleukin-12 expression on F4/80^(+)macrophages,as well as increasing interleukin-10 expression on CD4^(+)T cells and arginase-1,CD206,and interleukin-10 expression on F4/80^(+)macrophages,which improved immune regulation and reduced inflammation.These findings suggest that Fasudil-modified macrophages may help treat Experimental autoimmune encephalomyelitis by inducing M2 macrophage polarization and inhibiting the inflammatory response,thereby providing new insight into cell immunotherapy for multiple sclerosis.

关键词： anti-inflammatory Experimental autoimmune encephalomyelitis Fasudil macrophage multiple sclerosis pro-inflammatory Rho kinase