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experimental autoimmune encephalomyelitis Inhibited by Huangqi Guizhi Wuwu Decoction via Th2 Cytokine Enhancement

World Journal of Traditional Chinese Medicine 2021年第4期7卷 467-476页

作者： Yong Peng Fei-Zhou Zhu Xiang Deng Jian-Xiong Zhou Shuai Gao Zhi-Xing Chen Shan-Shan Yang Lu Gan Zhuo-Lin Li Qian-Qian Liu Department of Neurology Affiliated First Hospital of Hunan Traditional Chinese Medical CollegeZhuzhou Department of Biochemistry and Molecular Biology School of Life SciencesCentral South UniversityChangshaHunanChina

Background:Huangqi Guizhi Wuwu decoction(HQGZWW)exhibits good effects when administered to treat multiple sclerosis(MS)and its animal model,experimental autoimmune encephalomyelitis(EAE).Understanding the precise mechanism of this decoction is thus *** on the findings of our previous study,the aim of the present study was to understand the role of antigen-specific CD8^(+)T-cells on the pathogene sis of MS/EAE when HQGZWW is administered as ***:Myelin oligodendrocyte glycoprotein(MOG);-induced mice were administered distilled water,prednisone,and high dose or low dose *** purified CD4^(+)and CD8^(+)T-cells were stimulated with the MOG;peptide,proliferation and cytokine secretion assays were *** establish the adoptive transfer EAE model,naive mice were injected with MOG;-CD8^(+)or CD4^(+)***:Significant improvements in EAE score and pathology were observed in the high dose HQGZWW and prednisone *** to the low dose HQGZWW and distilled water groups,lower antigen-specific re sponses,lower levels of interferon-gamma,and higher levels of interleukin(IL)-4 and IL-10 from CD8^(+)and CD4^(+)T cells were observed in the high dose HQGZWW and prednisone ***,the EAE score was observed to be similar between the high dose HQGZWW group and prednisone group;however,this finding was not observed in the low dose HQGZWW ***:Our findings suggest that high dose HQGZWW has similar effects on cell proliferation,cytokine secretion,and EAE score to prednisone,while low dose HQGZWW does not have such *** protective role of HQGZWW against EAE might thus depend on the Th2 cytokine secretion profile induced by either MOG;specific CD8^(+)or CD4^(+)T-cells.

关键词： CD8-Positive T-lymphocytes experimental autoimmune encephalomyelitis multiple sclerosis myelin-oligodendrocyte glycoprotein Th2 cytokine traditional Chinese medicine

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Estrogen influences the differentiation, maturation and function of dendritic cells in rats with experimental autoimmune encephalomyelitis

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Acta Pharmacologica Sinica 2004年第4期25卷 110-115页

作者： Qing-hong ZHANG2, Yu-zhen HU, Jun CAO3, Yan-qing ZHONG,Yu-feng ZHAO, Qi-bing MEI4 Department of Physiology, Department ofOrthodontics, 3 4Department of Pharmacology, The Fourth Military Medical University, Xi’an 710032, China Department of Physiology The Fourth Military Medical University Xi'an 710032 China

AIM: To examine if estrogen can affect the immune response at the dendritic cells (DCs) level in rats with experi- mental autoimmune encephalomyelitis (EAE). METHODS: Lewis rats were immunized with inoculum containing MBP68-86. DCs were derived from spleen monocytes of EAE rats with IL-4 and GM-CSF in presence of 17β- estradiol (E2). Nitric oxide (NO) was detected by Griess reagent. The surface markers and cytokines production of DCs were shown by flow cytometry. DCs were cocultured with MBP-specific T cells, [3H]-TdR incoportation was used to reveal the antigen presentability, the supernatant of the coculture were collected to examine the cytokines secretion by ELISA. RESULTS: E2 activated DCs by accelerating the maturation process characterized by upregulation of MHC II and costimulating molecule B7-1, B7-2, drastic high expression of CD40. IFN-γ–produc- ing DCs were also elevated without any alteration of IL-10. Estradiol-treated DCs (E2-DCs) secreted more NO in the culture supernatant. By contrast, E2-DCs showed decreased antigen presentation ability with reduced secretion of IFN-γ but no alteration of IL-10 in the coculture with T cells. CONCLUSION: Estrogen can affect the differentiation, maturation and function of DCs from EAE rats, which may be attributed to its protection against EAE and the remission of multiple sclerosis patients in pregnancy.

关键词： multiple sclerosis experimental autoimmune encephalomyelitis dendritic cells estrogens nitric oxide

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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 *** the symptoms of MS can be managed by vitamin D3 treatment alone,this condition cannot be completely ***,there might be unknown factors capable of regulating the vitamin D receptor(VDR).Genome-wide analysis showed that miRNAs were associated with *** 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 *** mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control *** inflammatory infiltration was found in the lumbosacral spinal cord of EAE *** 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 ***,activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE ***,VDR and miR-125a-5p were co-localized in the same neurons of the ventral *** importantly,inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE *** 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

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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 is associated with relapsing-remitting multiple sclerosis,while progressive forms of the disease show axonal degeneration and neuronal *** tests currently used in the clinical diagnosis and management of multiple sclerosis have limitations due to specificity and ***(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 *** 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 *** using miRNA mimics or inhibitors were found to delay the induction and alleviate the severity of experimental autoimmune encephalomyelitis ***,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 *** 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 ***,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

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JAK inhibition ameliorated experimental autoimmune encephalomyelitis by blocking GM-CSF-driven inflammatory signature of monocytes

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Acta Pharmaceutica Sinica B 2023年第10期13卷 4185-4201页

作者： Shuai Shao Chengjuan Chen Gaona Shi Yu Zhou Yazi Wei Lei Wu Lan Sun Tiantai Zhang State Key Laboratory of Bioactive Substance and Function of Natural Medicines Institute of Materia MedicaChinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing 100050China

Monocytes are key effectors in autoimmunity-related diseases in the central nervous system(CNS)due to the critical roles of these cells in the production of proinflammatory cytokines,differentiation of T-helper(Th)cells,and antigen *** JAK-STAT signaling is crucial for initiating monocytes induced immune responses by relaying cytokines ***,the role of this pathway in modulating the communication between monocytes and Th cells in the pathogenesis of multiple sclerosis(MS)is ***,we show that the JAK1/2/3 and STAT1/3/5/6 subtypes involved in the demyelination mediated by the differentiation of pathological Th1 and Th17 and the CNS-infiltrating inflammatory monocytes in experimental autoimmune encephalomyelitis(EAE),a model for *** inhibition prevented the CNS-infiltrating CCR2-dependent Ly6^(Chi)monocytes and monocyte-derived dendritic cells in EAE *** parallel,the proportion of GM-CSF^(+)CD4^(+)T cells and GM-CSF secretion were decreased in pathological Th17 cells by JAK inhibition,which in turns converted CNS-invading monocytes into antigen-presenting cells to mediate tissue ***,our data highlight the therapeutic potential of JAK inhibition in treating EAE by blocking the GM-CSF-driven inflammatory signature of monocytes.

关键词： Monocytes T-helper cells Monocyte-derived dendritic cells GM-CSF JAK-STAT signaling JAK inhibitor experimental autoimmune encephalomyelitis Multiple sclerosis

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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 *** 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 ***,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 *** 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

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Pik3c3 deficiency in myeloid cells imparts partial resistance to experimental autoimmune encephalomyelitis associated with reduced IL-1βproduction

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Cellular & Molecular Immunology 2021年第8期18卷 2024-2039页

作者： Guan Yang Wenqiang Song Jielin Xu JLuke Postoak Feixiong Cheng Jennifer Martinez Jianhua Zhang Lan Wu Luc Van Kaer Department of Pathology Microbiology and ImmunologyVanderbilt University School of MedicineNashvilleTN37232USA Genomic Medicine Institute Lerner Research InstituteCleveland ClinicClevelandOH44195USA Department of Molecular Medicine Cleveland Clinic Lerner College of MedicineCase Western Reserve UniversityClevelandOH44195USA Case Comprehensive Cancer Center Case Western Reserve University School of MedicineClevelandOH44106USA Immunity Inflammationand Disease LaboratoryNational Institute of Environmental Health SciencesResearch Triangle ParkDurhamNC27709USA Department of Pathology University of Alabama at BirminghamBirminghamAL35294USA Birmingham Veterans Affairs Medical Center BirminghamAL35233USA

The PIK3C3/VPS34 subunit of the class III phosphatidylinositol 3-kinase(PtdIns3K)complex plays a role in both canonical and noncanonical autophagy,key processes that control immune-cell responsiveness to a variety of *** previous studies found that PIK3C3 is a critical regulator that controls the development,homeostasis,and function of dendritic and T *** this study,we investigated the role of PIK3C3 in myeloid cell biology using myeloid cell-specific Pik3c3-deficient *** found that Pik3c3-deficient macrophages express increased surface levels of major histocompatibility complex(MHC)class I and class II *** addition,myeloid cell-specific Pik3c3 ablation in mice caused a partial impairment in the homeostatic maintenance of macrophages expressing the apoptotic cell uptake receptor ***3c3 deficiency caused phenotypic changes in myeloid cells that were dependent on the early machinery(initiation/nucleation)of the classical autophagy ***,myeloid cell-specific Pik3c3-deficient animals showed significantly reduced severity of experimental autoimmune encephalomyelitis(EAE),a primarily CD4^(^(+))T-cell-mediated mouse model of multiple sclerosis(MS).This disease protection was associated with reduced accumulation of myelin-specific CD4^(^(+))T cells in the central nervous system and decreased myeloid cell IL-1β***,administration of SAR405,a selective PIK3C3 inhibitor,delayed disease ***,our studies establish PIK3C3 as an important regulator of macrophage functions and myeloid cell-mediated regulation of *** findings also have important implications for the development of small-molecule inhibitors of PIK3C3 as therapeutic modulators of MS and other autoimmune diseases.

关键词： PIK3C3 Autophagy Myeloid cells experimental autoimmune encephalomyelitis IL-1β

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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 e

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

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The circular RNA circINPP4B acts as a sponge of miR-30a to regulate Th17 cell differentiation during progression of experimental autoimmune encephalomyelitis

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Cellular & Molecular Immunology 2021年第9期18卷 2177-2187页

作者： Jingjing Han Wei Zhuang Wanhua Feng Fuxing Dong Fang Hua Ruiqin Yao Xuebin Qu Department of Cell Biology and Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsuChina Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsuChina Shanghai Key Laboratory of Signaling and Disease Research School of Life Sciences and TechnologyTongji UniversityShanghaiChina Institute of Neurological Diseases of Xuzhou Medical University XuzhouJiangsuChina

Circular RNAs(circRNAs)regulate gene expression and participate in various biological and pathological ***,little is known about the effects of specific circRNAs on T helper cell 17(Th17)differentiation and related autoimmune diseases,such as multiple sclerosis(MS).Here,using transcriptome microarray analysis at different stages of experimental autoimmune encephalomyelitis(EAE),we identified the EAE progression-related circINPP4B,which showed upregulated expression in Th17 cells from mice with EAE and during Th17 differentiation in *** of circINPP4B inhibited Th17 differentiation and alleviated EAE,characterized by less demyelination and Th17 infiltration in the spinal ***,circINPP4B served as a sponge that directly targeted miR-30a to regulate Th17 ***,circINPP4B levels were associated with the developing phases of clinical relapsing-remitting MS *** results indicate that circINPP4B plays an important role in promoting Th17 differentiation and progression of EAE by targeting miR-30a,which provides a potential diagnostic and therapeutic target for Th17-mediated MS.

关键词： Circular RNA Multiple sclerosis experimental autoimmune encephalomyelitis T helper cell miR-30a

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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 ***,the potential therapeutic effect of emodin in the context of multiple sclerosis remains *** 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 *** 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 *** 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 ***,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 *** 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

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