PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 16055951-3 2005 We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. N-Acetylcysteinamide 71-93 myelin oligodendrocyte glycoprotein Mus musculus 193-228 16426494-6 2005 Similar therapeutic effect by FTY720 was obtained in myelin oligodendrocyte glycoprotein-induced EAE in C57BL/6 mice. Fingolimod Hydrochloride 30-36 myelin oligodendrocyte glycoprotein Mus musculus 53-88 16098614-3 2005 We show that oral administration of the selective PPARdelta agonist GW0742 reduced clinical symptoms in C57BL/6 mice that had been immunized with encephalitogenic myelin oligodendrocyte glycoprotein (MOG) peptide. GW0742 68-74 myelin oligodendrocyte glycoprotein Mus musculus 163-198 16098614-3 2005 We show that oral administration of the selective PPARdelta agonist GW0742 reduced clinical symptoms in C57BL/6 mice that had been immunized with encephalitogenic myelin oligodendrocyte glycoprotein (MOG) peptide. GW0742 68-74 myelin oligodendrocyte glycoprotein Mus musculus 200-203 16055951-3 2005 We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. N-Acetylcysteinamide 71-93 myelin oligodendrocyte glycoprotein Mus musculus 230-233 16055951-3 2005 We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. N-Acetylcysteinamide 95-98 myelin oligodendrocyte glycoprotein Mus musculus 193-228 16055951-3 2005 We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. N-Acetylcysteinamide 95-98 myelin oligodendrocyte glycoprotein Mus musculus 230-233 16055951-5 2005 Therefore, we analyzed gene-expression profile in the spinal cords of MOG-induced chronic EAE mice and compared them with MOG-induced mice treated with AD4, using a cDNA microarray. N-Acetylcysteinamide 152-155 myelin oligodendrocyte glycoprotein Mus musculus 122-125 15680707-0 2005 Immunization with myelin oligodendrocyte glycoprotein and complete Freund adjuvant partially protects dopaminergic neurons from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced damage in mouse model of Parkinson"s disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 128-172 myelin oligodendrocyte glycoprotein Mus musculus 18-53 15681762-5 2004 The effect of GA was also tested in several models of CR-EAE: proteolipid protein and myelin oligodendrocyte glycoprotein induced CR-EAE in mice, CR-EAE in Biozzi mice, and CR-EAE in cynomolgus monkeys. cr-eae 130-136 myelin oligodendrocyte glycoprotein Mus musculus 86-121 15681762-5 2004 The effect of GA was also tested in several models of CR-EAE: proteolipid protein and myelin oligodendrocyte glycoprotein induced CR-EAE in mice, CR-EAE in Biozzi mice, and CR-EAE in cynomolgus monkeys. cr-eae 130-136 myelin oligodendrocyte glycoprotein Mus musculus 86-121 15681762-5 2004 The effect of GA was also tested in several models of CR-EAE: proteolipid protein and myelin oligodendrocyte glycoprotein induced CR-EAE in mice, CR-EAE in Biozzi mice, and CR-EAE in cynomolgus monkeys. cr-eae 130-136 myelin oligodendrocyte glycoprotein Mus musculus 86-121 15210763-4 2004 We show in this study that, in MOG:CFA-primed mice, the autoimmune CNS pathology develops after intracerebral deposition of TLR9-activating CpG oligonucleotides, but not following non-CpG oligonucleotide injection or after aseptic cryoinjury of the brain. Oligonucleotides 144-160 myelin oligodendrocyte glycoprotein Mus musculus 31-34 15210763-4 2004 We show in this study that, in MOG:CFA-primed mice, the autoimmune CNS pathology develops after intracerebral deposition of TLR9-activating CpG oligonucleotides, but not following non-CpG oligonucleotide injection or after aseptic cryoinjury of the brain. Oligonucleotides 144-159 myelin oligodendrocyte glycoprotein Mus musculus 31-34 15081244-2 2004 Preventive treatment of experimental autoimmune encephalomyelitis (EAE)-induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55-with the NO-releasing derivative of flurbiprofen HCT1026 delayed disease onset and significantly decreased disease severity. Flurbiprofen 209-221 myelin oligodendrocyte glycoprotein Mus musculus 117-152 15147517-5 2004 In agreement with the in vitro studies, we propose that ROS scavenging by AD4 in MOG-treated animals prevented MMP"s induction and subsequent damages through inhibition of MAPK pathway. Reactive Oxygen Species 56-59 myelin oligodendrocyte glycoprotein Mus musculus 81-84 15081244-2 2004 Preventive treatment of experimental autoimmune encephalomyelitis (EAE)-induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55-with the NO-releasing derivative of flurbiprofen HCT1026 delayed disease onset and significantly decreased disease severity. Flurbiprofen 209-221 myelin oligodendrocyte glycoprotein Mus musculus 154-157 14768043-7 2004 Therefore, MOG 35-55-specific precursors stimulated with a weak ligand (45D) mediate some EAE-associated effector functions but are unable to fully initiate the inflammatory process in the central nervous system that leads to clinical manifestation of EAE. EAE 90-93 myelin oligodendrocyte glycoprotein Mus musculus 11-14 15051763-7 2004 Disease prevention correlates with the ability of sulfatide to suppress both interferon-gamma and interleukin-4 production by pathogenic myelin oligodendrocyte glycoprotein-reactive T cells. Sulfoglycosphingolipids 50-59 myelin oligodendrocyte glycoprotein Mus musculus 137-172 12395089-3 2002 We report that, whereas approximately 50% of optic nerve axons are lost at 27-28 days in untreated EAE, only approximately 12% of the axons are lost if mice with MOG-induced EAE are treated with phenytoin. Phenytoin 195-204 myelin oligodendrocyte glycoprotein Mus musculus 162-165 14556941-2 2003 Therefore, we examined whether riluzole, an inhibitor of glutamate transmission, affects the pathogenesis and clinical features of MS-like disease in myelin oligodendrocyte glycoprotein (MOG)-induced EAE in mice. Riluzole 31-39 myelin oligodendrocyte glycoprotein Mus musculus 187-190 14556941-8 2003 In conclusion, our study demonstrates, for the first time, that riluzole can reduce inflammation, demyelination and axonal damage in the CNS and attenuate the clinical severity of MOG-induced EAE. Riluzole 64-72 myelin oligodendrocyte glycoprotein Mus musculus 180-183 12926537-0 2003 Post intoxicative therapeutic immunization with myelin oligodendrocyte glycoproteine (MOG 35-55) suppresses spontaneous regeneration of dopaminergic neurons injured with 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine (MPTP). 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine 170-214 myelin oligodendrocyte glycoprotein Mus musculus 86-89 12926537-0 2003 Post intoxicative therapeutic immunization with myelin oligodendrocyte glycoproteine (MOG 35-55) suppresses spontaneous regeneration of dopaminergic neurons injured with 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridine (MPTP). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 216-220 myelin oligodendrocyte glycoprotein Mus musculus 86-89 12778471-3 2003 Our study demonstrates that DBA/1 mice could be protected from experimental autoimmune encephalomyelitis induced through injection of recombinant myelin oligodendrocyte glycoprotein (rMOG) when they were previously immunized intraperitoneally with rMOG adsorbed to aluminium hydroxide. Aluminum Hydroxide 265-284 myelin oligodendrocyte glycoprotein Mus musculus 146-181 12112074-3 2002 We demonstrate in two models of EAE that orally administered PPARgamma ligand pioglitazone reduced the incidence and severity of monophasic, chronic disease in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein peptide and of relapsing disease in B10.Pl mice immunized with myelin basic protein. Pioglitazone 78-90 myelin oligodendrocyte glycoprotein Mus musculus 188-223 11438174-0 2001 Brain-derived gangliosides suppress the chronic relapsing-remitting experimental autoimmune encephalomyelitis in NOD mice induced with myelin oligodendrocyte glycoprotein peptide. Gangliosides 14-26 myelin oligodendrocyte glycoprotein Mus musculus 135-170 12023389-7 2002 Specific inhibition of NO production in vivo by treatment with the inducible NO synthase inhibitor, L-N(6)-(1-iminoethyl)-lysine, suppressed circulating nitrites, increased myelin oligodendrocyte glycoprotein-specific cell proliferation, and rendered GR-deficient mice susceptible to EAE. N(6)-(1-iminoethyl)lysine 100-128 myelin oligodendrocyte glycoprotein Mus musculus 173-208 11390514-2 2001 In this study, we report that synthetic peptides 35-55 from myelin oligodendrocyte glycoprotein (pMOG(35-55)) consistently activate a high proportion of CD8+ alphabetaTCR+ T cells that are encephalitogenic in C57BL/6 (B6) mice. Peptides 40-48 myelin oligodendrocyte glycoprotein Mus musculus 60-95 11438174-1 2001 Chronic relapsing-remitting experimental autoimmune encephalomyelitis (CREAE) induced with myelin oligodendrocyte glycoprotein peptides 35-55 (MOG(35-55)) in NOD mice was successfully treated with brain-derived gangliosides (GA). Gangliosides 211-223 myelin oligodendrocyte glycoprotein Mus musculus 91-126 11438174-3 2001 Spleen cells from the GA-treated mice displayed markedly inhibited levels of MOG(35-55) specific proliferation and interferon-gamma production. Gangliosides 22-24 myelin oligodendrocyte glycoprotein Mus musculus 77-80 11311328-3 2001 In the present study, we examined whether troglitazone, a selective PPAR-gamma agonists, ameliorated experimental autoimmune encephalomyelitis (EAE) induced by administration of myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 in C57BL/6 mice. Troglitazone 42-54 myelin oligodendrocyte glycoprotein Mus musculus 178-213 11311328-3 2001 In the present study, we examined whether troglitazone, a selective PPAR-gamma agonists, ameliorated experimental autoimmune encephalomyelitis (EAE) induced by administration of myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 in C57BL/6 mice. Troglitazone 42-54 myelin oligodendrocyte glycoprotein Mus musculus 215-218 9143251-2 1997 Here we describe the induction of EAE in SJL and (PLJ X SJL)F1 mice with truncated human recombinant MOG (thr-MOG, amino acids 1-120) which has been expressed in insect cells in soluble form. Threonine 106-109 myelin oligodendrocyte glycoprotein Mus musculus 110-113 11122253-5 2000 A significant increase in the production of TGF-beta1 in response to concanavalin A (Con A) at day 13 and a significant increase in TGF-beta1 and PGE2 to Con A, PPD and MOG peptide (92-106) at day 21 were detected in spleen mononuclear cells from fatty acid-fed mice. Dinoprostone 146-150 myelin oligodendrocyte glycoprotein Mus musculus 169-172 10064079-7 1999 Taken together these findings define TNFR1 as crucial mediator in MOG-induced EAE and suggest a protective role for TNFR2 signaling in the clinical course of EAE. EAE 78-81 myelin oligodendrocyte glycoprotein Mus musculus 66-69 10741394-3 2000 EAE was induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55. EAE 0-3 myelin oligodendrocyte glycoprotein Mus musculus 53-88 9143251-3 1997 We show that in SJL mice, immunization with thr-MOG produces an immune response to the 1-30 and the 81-110 regions of the MOG molecule. Threonine 44-47 myelin oligodendrocyte glycoprotein Mus musculus 48-51 9143251-3 1997 We show that in SJL mice, immunization with thr-MOG produces an immune response to the 1-30 and the 81-110 regions of the MOG molecule. Threonine 44-47 myelin oligodendrocyte glycoprotein Mus musculus 122-125 9143251-4 1997 We also demonstrate effective treatment of thr-MOG-induced EAE in SJL mice with intravenous injections of a single peptide, MOG 91-110. Threonine 43-46 myelin oligodendrocyte glycoprotein Mus musculus 47-50 9143251-4 1997 We also demonstrate effective treatment of thr-MOG-induced EAE in SJL mice with intravenous injections of a single peptide, MOG 91-110. Threonine 43-46 myelin oligodendrocyte glycoprotein Mus musculus 124-127 34748963-3 2022 The brain autoantigen, myelin oligodendrocyte glycoprotein (MOG), was conjugated to 200 or 500nm silica nanoparticles (SNP) and delivered to the spleen and liver-resident macrophages of experimental autoimmune encephalomyelitis (EAE) mice model of multiple sclerosis. Silicon Dioxide 97-103 myelin oligodendrocyte glycoprotein Mus musculus 60-63 1373175-7 1992 MOG was purified by polyacrylamide gel electrophoresis, followed by electroelution. polyacrylamide 20-34 myelin oligodendrocyte glycoprotein Mus musculus 0-3 34310708-3 2021 Patients with multiple sclerosis (MS) are reported to have elevated blood levels of ADMA and mice with experimental autoimmune encephalomyelitis (EAE, an animal model of MS) generated by auto-immunization of myelin oligodendrocyte glycoprotein (MOG) and blood-brain barrier (BBB) disruption by pertussis toxin also had increased blood ADMA levels in parallel with induction of clinical disease. N,N-dimethylarginine 335-339 myelin oligodendrocyte glycoprotein Mus musculus 208-243 34310708-6 2021 ADMA treatment also induced the BBB disruption and EAE disease in MOG-immunized mice even without pertussis toxin treatment, suggesting the role of ADMA in BBB dysfunction in EAE. N,N-dimethylarginine 0-4 myelin oligodendrocyte glycoprotein Mus musculus 66-69 34310708-3 2021 Patients with multiple sclerosis (MS) are reported to have elevated blood levels of ADMA and mice with experimental autoimmune encephalomyelitis (EAE, an animal model of MS) generated by auto-immunization of myelin oligodendrocyte glycoprotein (MOG) and blood-brain barrier (BBB) disruption by pertussis toxin also had increased blood ADMA levels in parallel with induction of clinical disease. N,N-dimethylarginine 335-339 myelin oligodendrocyte glycoprotein Mus musculus 245-248 34310708-6 2021 ADMA treatment also induced the BBB disruption and EAE disease in MOG-immunized mice even without pertussis toxin treatment, suggesting the role of ADMA in BBB dysfunction in EAE. N,N-dimethylarginine 148-152 myelin oligodendrocyte glycoprotein Mus musculus 66-69 34513625-3 2021 Some efforts have been made to bioconjugate the MOG peptides to tolerogenic particles like poly (lactic-co-glycolic acid) (PLGA) for treating animal models of autoimmune disorders. Polylactic Acid-Polyglycolic Acid Copolymer 91-121 myelin oligodendrocyte glycoprotein Mus musculus 48-51 34232258-2 2021 Methods: EAON was induced in mice via subcutaneous injection with myelin oligodendrocyte glycoprotein peptide. eaon 9-13 myelin oligodendrocyte glycoprotein Mus musculus 66-101 34748963-3 2022 The brain autoantigen, myelin oligodendrocyte glycoprotein (MOG), was conjugated to 200 or 500nm silica nanoparticles (SNP) and delivered to the spleen and liver-resident macrophages of experimental autoimmune encephalomyelitis (EAE) mice model of multiple sclerosis. Silicon Dioxide 97-103 myelin oligodendrocyte glycoprotein Mus musculus 23-58 34513625-3 2021 Some efforts have been made to bioconjugate the MOG peptides to tolerogenic particles like poly (lactic-co-glycolic acid) (PLGA) for treating animal models of autoimmune disorders. Polylactic Acid-Polyglycolic Acid Copolymer 123-127 myelin oligodendrocyte glycoprotein Mus musculus 48-51 35330085-0 2022 EGF-Coupled Gold Nanoparticles Increase the Expression of CNPase and the Myelin-Associated Proteins MAG, MOG, and MBP in the Septal Nucleus Demyelinated by Cuprizone. Cuprizone 156-165 myelin oligodendrocyte glycoprotein Mus musculus 105-108 35018577-6 2022 PIGA1138 (15 mg/kg) drastically reduced MOG-EAE mice clinical scores, ameliorated motor dysfunctions assessed with the Catwalk device, and counteracted MOG-EAE-induced demyelination by preserving Myelin basic protein (MBP) expression in the CNS. piga1138 0-8 myelin oligodendrocyte glycoprotein Mus musculus 40-43 35018577-9 2022 Concordantly, PIGA1138 enhanced anti-inflammatory interleukin-10 serum level in MOG-EAE mice. piga1138 14-22 myelin oligodendrocyte glycoprotein Mus musculus 80-83 35384725-0 2022 Effect of Rapamycin on MOG-Reactive Immune Cells and Lipopolysaccharide-Activated Microglia: An In Vitro Approach for Screening New Therapies for Multiple Sclerosis. Sirolimus 10-19 myelin oligodendrocyte glycoprotein Mus musculus 23-26 35384725-2 2022 In this study, we evaluated the in vitro effect of rapamycin on immune cells pivotally involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is an animal model to study MS. Splenocytes and central nervous system (CNS)-mononuclear cells obtained from EAE mice were stimulated with a myelin oligodendrocyte glycoprotein peptide, whereas the microglial BV-2 cell line was activated with LPS. Sirolimus 51-60 myelin oligodendrocyte glycoprotein Mus musculus 315-350 33189793-3 2021 NEW METHOD: A detailed and systematic titration of the MOG 35-55 EAE induction protocol in C57BL/6 mice reveals the minimal doses of the MOG 35-55 peptide, MT H37Ra, and PTx, required for disease manifestation. Peptides 147-154 myelin oligodendrocyte glycoprotein Mus musculus 137-140 34033858-5 2021 Additionally, invasion of inflammatory immune cells into the spinal cord and demyelination of neurons were clearly suppressed in the MOG-LipDOX-treated mice. lipdox 137-143 myelin oligodendrocyte glycoprotein Mus musculus 133-136 33595155-5 2021 The effect of ACT-1004-1239 was evaluated in the myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) and the cuprizone-induced demyelination mouse models. CHEMBL4782111 14-27 myelin oligodendrocyte glycoprotein Mus musculus 86-89 35076460-3 2022 Previously we showed that TCDD inhibited myelin oligodendrocyte glycoprotein (MOG) peptide-specific IgG and attenuated disease in experimental autoimmune encephalomyelitis (EAE) model in mice. Polychlorinated Dibenzodioxins 26-30 myelin oligodendrocyte glycoprotein Mus musculus 41-76 35076460-3 2022 Previously we showed that TCDD inhibited myelin oligodendrocyte glycoprotein (MOG) peptide-specific IgG and attenuated disease in experimental autoimmune encephalomyelitis (EAE) model in mice. Polychlorinated Dibenzodioxins 26-30 myelin oligodendrocyte glycoprotein Mus musculus 78-81 35076460-9 2022 Lastly, we revisited the EAE model and determined that TCDD suppressed MOG-specific IgG1 production. Polychlorinated Dibenzodioxins 55-59 myelin oligodendrocyte glycoprotein Mus musculus 71-74 34025136-4 2021 Methods: Here, we investigated whether Rg3-KRGE may improve the symptoms and pathological features of myelin oligodendroglial glycoprotein (MOG)35-55 peptide - induced chronic EAE mice through improving the integrity of the BBB. ginsenoside Rg3 39-42 myelin oligodendrocyte glycoprotein Mus musculus 140-143 34025136-4 2021 Methods: Here, we investigated whether Rg3-KRGE may improve the symptoms and pathological features of myelin oligodendroglial glycoprotein (MOG)35-55 peptide - induced chronic EAE mice through improving the integrity of the BBB. Peptides 150-157 myelin oligodendrocyte glycoprotein Mus musculus 140-143 33345977-5 2021 Activin receptor type I (ACVR1) inhibitor SB431542 aggregated neurological deficits, and reduced MAG, MOG and MBP protein levels of mice with ischemic stroke (n = 6 per group). 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 42-50 myelin oligodendrocyte glycoprotein Mus musculus 102-105 32812186-3 2021 In this study, possible beneficial effects of sinomenine in an MOG-induced model of MS were determined. sinomenine 46-56 myelin oligodendrocyte glycoprotein Mus musculus 63-66 32812186-7 2021 Furthermore, immunoreactivity for MBP decreased and increased for GFAP and Iba1 after MOG-immunization, which was in part reversed upon sinomenine administration. sinomenine 136-146 myelin oligodendrocyte glycoprotein Mus musculus 86-89 33157256-8 2021 Expression of myelin-related genes (Mag, Mog, Mbp, Mobp, Plp) and transcription factors (Sox10, Myrf) important for oligodendrocytes were significantly increased in the PFC region of Abx-treated mice. CHEMBL369125 183-186 myelin oligodendrocyte glycoprotein Mus musculus 41-44 33490940-5 2021 A-1396076 inhibited antigen dependent T cell activation as measured by IFN-gamma production in an ex vivo re-stimulation assay and following anti-CD3 challenge of MOG-sensitized mice. a-1396076 0-9 myelin oligodendrocyte glycoprotein Mus musculus 163-166 32615414-8 2020 Further, the adoptive transfer of B cells incubated with FITC-labeled myelin oligodendrocyte glycoprotein peptide protected mice from experimental autoimmune encephalomyelitis, a T-cell-dependent autoimmune model. Fluorescein-5-isothiocyanate 57-61 myelin oligodendrocyte glycoprotein Mus musculus 70-105 33066323-0 2020 Characterization of Asparagine Deamidation in Immunodominant Myelin Oligodendrocyte Glycoprotein Peptide Potential Immunotherapy for the Treatment of Multiple Sclerosis. Asparagine 20-30 myelin oligodendrocyte glycoprotein Mus musculus 61-96 33066323-1 2020 Mannan (polysaccharide) conjugated with a myelin oligodendrocyte glycoprotein (MOG) peptide, namely (KG)5MOG35-55, represents a potent and promising new approach for the immunotherapy of Multiple Sclerosis (MS). Mannans 0-6 myelin oligodendrocyte glycoprotein Mus musculus 42-77 33066323-1 2020 Mannan (polysaccharide) conjugated with a myelin oligodendrocyte glycoprotein (MOG) peptide, namely (KG)5MOG35-55, represents a potent and promising new approach for the immunotherapy of Multiple Sclerosis (MS). Mannans 0-6 myelin oligodendrocyte glycoprotein Mus musculus 79-82 33066323-1 2020 Mannan (polysaccharide) conjugated with a myelin oligodendrocyte glycoprotein (MOG) peptide, namely (KG)5MOG35-55, represents a potent and promising new approach for the immunotherapy of Multiple Sclerosis (MS). Polysaccharides 8-22 myelin oligodendrocyte glycoprotein Mus musculus 42-77 33066323-1 2020 Mannan (polysaccharide) conjugated with a myelin oligodendrocyte glycoprotein (MOG) peptide, namely (KG)5MOG35-55, represents a potent and promising new approach for the immunotherapy of Multiple Sclerosis (MS). Polysaccharides 8-22 myelin oligodendrocyte glycoprotein Mus musculus 79-82 33066323-6 2020 Our results demonstrate that the synthesized MOG peptides were formed to the deaminated products in basic conditions, and the Asn53 was mainly modified to Asp. Aspartic Acid 155-158 myelin oligodendrocyte glycoprotein Mus musculus 45-48 32329062-7 2020 Our results showed that the maximum mean clinical score and myelin oligodendrocyte glycoprotein-induced proliferation of splenocytes in hADSC- and hADSC-EV-treated mice were significantly lower than the control mice (p < .05). hadsc 136-141 myelin oligodendrocyte glycoprotein Mus musculus 60-95 32329062-7 2020 Our results showed that the maximum mean clinical score and myelin oligodendrocyte glycoprotein-induced proliferation of splenocytes in hADSC- and hADSC-EV-treated mice were significantly lower than the control mice (p < .05). hadsc-ev 147-155 myelin oligodendrocyte glycoprotein Mus musculus 60-95 33193354-3 2020 Since new control measures remain necessary, we evaluated the preventive and therapeutic potential of a beta-selenium-lactic acid derivative (LAD-betaSe), which is a source of organic selenium under development, to control experimental autoimmune encephalomyelitis (EAE) that is an animal model for MS. Two EAE murine models: C57BL/6 and SJL/J immunized with myelin oligodendrocyte glycoprotein and proteolipid protein, respectively, and a model of neurodegeneration induced by LPS in male C57BL/6 mice were used. beta-selenium 104-117 myelin oligodendrocyte glycoprotein Mus musculus 359-394 33193354-3 2020 Since new control measures remain necessary, we evaluated the preventive and therapeutic potential of a beta-selenium-lactic acid derivative (LAD-betaSe), which is a source of organic selenium under development, to control experimental autoimmune encephalomyelitis (EAE) that is an animal model for MS. Two EAE murine models: C57BL/6 and SJL/J immunized with myelin oligodendrocyte glycoprotein and proteolipid protein, respectively, and a model of neurodegeneration induced by LPS in male C57BL/6 mice were used. Lactic Acid 118-129 myelin oligodendrocyte glycoprotein Mus musculus 359-394 32353424-7 2020 Finally, piperine exhibits strong preventive and therapeutic effect in the MOG-induced experimental allergic encephalomyelitis (EAE), a useful model for studying potential treatments for MS, by restricting inflammatory cells infiltration into the CNS and preventing myelin destruction and blood-brain barrier (BBB) disruption. piperine 9-17 myelin oligodendrocyte glycoprotein Mus musculus 75-78 32448554-0 2020 Retraction notice to "Hydroxyfasudil alleviates demyelination through the inhibition of MOG antibody and microglia activation in cuprizone mouse model" [Clin. hydroxyfasudil 22-36 myelin oligodendrocyte glycoprotein Mus musculus 88-91 32448554-0 2020 Retraction notice to "Hydroxyfasudil alleviates demyelination through the inhibition of MOG antibody and microglia activation in cuprizone mouse model" [Clin. Cuprizone 129-138 myelin oligodendrocyte glycoprotein Mus musculus 88-91 31916130-6 2020 Our results demonstrated that CPZ-induced demyelination induces apparent alterations in the expression of most of the myelin-related genes, including the 6 key genes MBP, MAG, and MOG and GFAP, CXCR4, and NgR, which were observed to be downregulated and upregulated, respectively, suggesting that the differences in gene expression in vivo could serve as potential therapeutic targets for remyelination. Cuprizone 30-33 myelin oligodendrocyte glycoprotein Mus musculus 180-183 32522287-8 2020 Conversely, the low-efficiency GMCSF-MOG vaccine lacked adequate TCR signal strength to elicit CD40L expression and instead elicited Tregs by a mechanism that was impaired by a CD40 agonist. tregs 133-138 myelin oligodendrocyte glycoprotein Mus musculus 37-40 32522287-11 2020 Subcutaneous administration of GMCSF-MOG without adjuvants inhibited EAE in wildtype mice, which had a replete Treg repertoire, but was pathogenic rather than tolerogenic in 2D2-FIG-Rag1-/- mice, which lacked pre-existing Tregs. tregs 222-227 myelin oligodendrocyte glycoprotein Mus musculus 37-40 32337654-1 2020 The objective of this work was to investigate the capacity of mogroside V (MOG-V), a food additive, as a novel carrier to improve the bioavailability and liver distribution of silybin (SLY). mogroside V 62-73 myelin oligodendrocyte glycoprotein Mus musculus 75-78 32337654-1 2020 The objective of this work was to investigate the capacity of mogroside V (MOG-V), a food additive, as a novel carrier to improve the bioavailability and liver distribution of silybin (SLY). Silybin 176-183 myelin oligodendrocyte glycoprotein Mus musculus 75-78 32337654-1 2020 The objective of this work was to investigate the capacity of mogroside V (MOG-V), a food additive, as a novel carrier to improve the bioavailability and liver distribution of silybin (SLY). Silybin 185-188 myelin oligodendrocyte glycoprotein Mus musculus 75-78 32010149-10 2019 Further, in vivo blockade of Treg accelerated the onset of symptoms in 1C6 mice immunized with MOG[35-55], indicating the pertinence of Treg-mediated control of autoimmune inflammation in this model. treg 29-33 myelin oligodendrocyte glycoprotein Mus musculus 95-98 32222873-5 2020 H-cKO mice responded normally to innate and passively induced inflammation, but showed significantly increased morbidity in T cell-dependent house dust mite-antigen (HDM)-induced asthma and myelin oligodendrocyte glycoprotein (MOG) peptide-induced experimental autoimmune encephalomyelitis (EAE). CKO 2-5 myelin oligodendrocyte glycoprotein Mus musculus 190-225 32222873-5 2020 H-cKO mice responded normally to innate and passively induced inflammation, but showed significantly increased morbidity in T cell-dependent house dust mite-antigen (HDM)-induced asthma and myelin oligodendrocyte glycoprotein (MOG) peptide-induced experimental autoimmune encephalomyelitis (EAE). CKO 2-5 myelin oligodendrocyte glycoprotein Mus musculus 227-230 32474563-8 2020 The gene expression patterns of Mag, Mog, and Cnp, which played key roles in myelination, were significantly changed with the treatment of 2-MesADP. methylthio-ADP 139-147 myelin oligodendrocyte glycoprotein Mus musculus 37-40 31124292-8 2020 In addition, Fasudil inhibited the production of myelin oligodendrocyte glycoprotein antibody and the infiltration of peripheral CD4+ T cells and CD68+ macrophages, which appears to be related to the integrity of the blood-brain barrier. fasudil 13-20 myelin oligodendrocyte glycoprotein Mus musculus 49-84 31620963-7 2019 RESULTS: Our finding indicated that consumption of metformin during the recovery period potentially induced an active form of AMPK (p-AMPK) and promoted repopulation of mature OLGs (MOG+ cells, MBP+ cells) in CC through up-regulation of BDNF, CNTF, and NGF as well as down-regulation of NogoA and recruitment of Olig2+ precursor cells. Metformin 51-60 myelin oligodendrocyte glycoprotein Mus musculus 182-185 31463682-9 2020 Ket also triggered an evident lymphadenomegaly due to accumulation of T cells that produced higher levels of encephalitogenic cytokines in response to in vitro stimulation with MOG. Ketotifen 0-3 myelin oligodendrocyte glycoprotein Mus musculus 177-180 29536745-3 2018 METHODS: The astaxanthin potential in prevention of multiple sclerosis was examined in the chronic model of experimental autoimmune encephalomyelitis (EAE) by using female C57BL/6 mice induced with oligodendrocyte glycoprotein (MOG). astaxanthine 13-24 myelin oligodendrocyte glycoprotein Mus musculus 228-231 31226280-2 2019 In the present study, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice were treated with adenosine receptor A2A antagonist SCH58261 at different periods of EAE development. 5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine 177-185 myelin oligodendrocyte glycoprotein Mus musculus 22-57 31226280-2 2019 In the present study, myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice were treated with adenosine receptor A2A antagonist SCH58261 at different periods of EAE development. 5-amino-7-(2-phenylethyl)-2-(2-furyl)pyrazolo(4,3-e)-1,2,4-triazolo(1,5-c)pyrimidine 177-185 myelin oligodendrocyte glycoprotein Mus musculus 59-62 31016368-4 2019 Here, we describe that in spite of its immunosuppressive effects, a continuous intoxication with cuprizone allows the induction of active experimental autoimmune encephalomyelitis (EAE) by myelin oligodendrocyte glycoprotein (MOG35-55) immunization. Cuprizone 97-106 myelin oligodendrocyte glycoprotein Mus musculus 189-224 30660624-0 2019 Hydroxyfasudil alleviates demyelination through the inhibition of MOG antibody and microglia activation in cuprizone mouse model. hydroxyfasudil 0-14 myelin oligodendrocyte glycoprotein Mus musculus 66-69 30660624-0 2019 Hydroxyfasudil alleviates demyelination through the inhibition of MOG antibody and microglia activation in cuprizone mouse model. Cuprizone 107-116 myelin oligodendrocyte glycoprotein Mus musculus 66-69 30873027-4 2019 Results showed that melatonin decreased neurological disability scores and enhanced remyelination, significantly increasing myelin protein levels including MBP, MOG, and MOBP. Melatonin 20-29 myelin oligodendrocyte glycoprotein Mus musculus 161-164 30572255-5 2019 RESULTS: Treatment by disease-inducing peptide (MOG35-55) combined with MSC-EXO or by MOG+TEX enhanced the expression of Foxp3 as the master regulator for Treg cells; by comparing with splenocytes which were treated by MOG. NSC643817 90-93 myelin oligodendrocyte glycoprotein Mus musculus 86-89 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Melatonin 20-29 myelin oligodendrocyte glycoprotein Mus musculus 156-191 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Melatonin 20-29 myelin oligodendrocyte glycoprotein Mus musculus 193-196 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Melatonin 31-34 myelin oligodendrocyte glycoprotein Mus musculus 156-191 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Melatonin 31-34 myelin oligodendrocyte glycoprotein Mus musculus 193-196 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Baclofen 65-73 myelin oligodendrocyte glycoprotein Mus musculus 156-191 29497878-4 2018 Results showed that melatonin (Mel) alone or in combination with baclofen (Bac + Mel) reduced clinical scores and demyelination by significantly increasing myelin oligodendrocyte glycoprotein (MOG) levels, a marker for mature oligodendrocytes, compared to EAE mice. Baclofen 65-73 myelin oligodendrocyte glycoprotein Mus musculus 193-196 28776122-4 2018 Using myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) as a MS model, we previously showed that daily administration of sildenafil starting at peak disease rapidly ameliorates clinical symptoms while administration at symptoms onset prevents disease progression. Sildenafil Citrate 169-179 myelin oligodendrocyte glycoprotein Mus musculus 6-41 28776122-4 2018 Using myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) as a MS model, we previously showed that daily administration of sildenafil starting at peak disease rapidly ameliorates clinical symptoms while administration at symptoms onset prevents disease progression. Sildenafil Citrate 169-179 myelin oligodendrocyte glycoprotein Mus musculus 43-46 29471880-2 2018 We aimed to evaluate an xc-specific positron emission tomography (PET) radiotracer, (4S)-4-(3-[18F]fluoropropyl)-L-glutamate ([18F]FSPG), for its ability to allow non-invasive monitoring of xc- activity in a mouse model of MS. METHODS: Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice by subcutaneous injection of myelin oligodendrocyte glycoprotein (MOG35-55) peptide in complete Freund"s adjuvant (CFA) followed by pertussis toxin. (4S)-4-(3-(18F)fluoropropyl)-L-glutamate 84-124 myelin oligodendrocyte glycoprotein Mus musculus 341-376 31489534-5 2019 Co-administration of cup and YM155 (cuYM) accelerated the intrinsic apoptosis of mature OLGs (MOG positive cells) through the upregulation of caspase-9 and caspase-3. YM 155 29-34 myelin oligodendrocyte glycoprotein Mus musculus 94-97 30738572-6 2019 MOG-MIFA immunized mice showed an early disease onset and more severe clinical scores in comparison with MOG-CFA immunized mice, demonstrating for the first time the adjuvant effect of MAP on EAE development. mifa 4-8 myelin oligodendrocyte glycoprotein Mus musculus 0-3 30738572-6 2019 MOG-MIFA immunized mice showed an early disease onset and more severe clinical scores in comparison with MOG-CFA immunized mice, demonstrating for the first time the adjuvant effect of MAP on EAE development. 3-chloro-4-fluoroaniline 109-112 myelin oligodendrocyte glycoprotein Mus musculus 105-108 30684521-8 2019 RESULTS: All EAE-MOG animals showed presence of LMCE and none of the control mice. lmce 48-52 myelin oligodendrocyte glycoprotein Mus musculus 17-20 30684521-14 2019 CONCLUSIONS: LMCE peak intensity in the meninges corresponds to the acute inflammatory phase of EAE-MOG disease progression, and is associated with clinical symptoms and higher inflammatory cell density. lmce 13-17 myelin oligodendrocyte glycoprotein Mus musculus 100-103 30820608-5 2019 RESULTS: Interestingly, celastrol reversed the expression of many MOG-induced genes involved in inflammation and immune pathology. celastrol 24-33 myelin oligodendrocyte glycoprotein Mus musculus 66-69 31066255-7 2019 MOG/chitin stimulation resulted in a significant increase in IFN-gamma and IL-10 levels, respectively; (p<=0.004 and p<=0.003) rather than MOG. Chitin 4-10 myelin oligodendrocyte glycoprotein Mus musculus 0-3 31066255-8 2019 Additionally, the expression of Tbx21 (p<=0.001), but not Gata3 (p<=0.08), was increased in the MOG/chitin-treated spleen cells. Chitin 106-112 myelin oligodendrocyte glycoprotein Mus musculus 102-105 30687323-5 2018 Notably, a single subcutaneous vaccination of GMCSF-MOG in saline elicited a major population of FOXP3+ Tregs that appeared within 3 days, was sustained over several weeks, expressed canonical Treg markers, and was present systemically at high frequencies in the blood, spleen, and lymph nodes. Sodium Chloride 59-65 myelin oligodendrocyte glycoprotein Mus musculus 52-55 30687323-12 2018 Comparison of 2D2-FIG and 2D2-FIG-Rag1 -/- strains revealed that GMCSF-MOG may predominantly drive Treg expansion because the kinetics of vaccine-induced Treg emergence was a function of pre-existing Treg levels. treg 99-103 myelin oligodendrocyte glycoprotein Mus musculus 71-74 29394220-0 2018 Beneficial effect of atorvastatin-modified dendritic cells pulsed with myelin oligodendrocyte glycoprotein autoantigen on experimental autoimmune encephalomyelitis. Atorvastatin 21-33 myelin oligodendrocyte glycoprotein Mus musculus 71-106 29394220-7 2018 Taken together, TolDCs-MOG modified by atorvastatin showed a characteristic tolerogenic phenotype and the antigen-specific TolDCs might represent a new promising strategy for the future treatments for multiple sclerosis. Atorvastatin 39-51 myelin oligodendrocyte glycoprotein Mus musculus 16-26 28759565-7 2017 Injection of CTlo- or cAMP-DCs exerted MOG peptide-specific protective effects in experimental autoimmune encephalomyelitis (EAE) by inducing Foxp3+ Tregs and reducing Th17 responses. Cyclic AMP 22-26 myelin oligodendrocyte glycoprotein Mus musculus 39-42 29066789-6 2017 In a murine model of multiple sclerosis, experimental autoimmune encephalopathy, 14-dehydroergosterol suppressed the clinical score and inflammatory responses of myeloid DCs and T cells to myelin oligodendrocyte glycoprotein. (22E,24S)-24-methylcholesta-5,7,14,22-tetraen-3beta-ol 81-101 myelin oligodendrocyte glycoprotein Mus musculus 189-224 30534814-4 2018 In this study, we aimed to evaluate the motor function, as well as the degree of demyelination and inflammatory changes in the brains of mice immunized for the myelin oligodendrocyte glycoprotein (MOG)35-55, and treated with Cerebrolysin. cerebrolysin 225-237 myelin oligodendrocyte glycoprotein Mus musculus 160-195 30534814-4 2018 In this study, we aimed to evaluate the motor function, as well as the degree of demyelination and inflammatory changes in the brains of mice immunized for the myelin oligodendrocyte glycoprotein (MOG)35-55, and treated with Cerebrolysin. cerebrolysin 225-237 myelin oligodendrocyte glycoprotein Mus musculus 197-200 28851628-5 2017 The highly PDE8-selective enzymatic inhibitor PF-04957325 suppresses adhesion of in vivo myelin oligodendrocyte glycoprotein (MOG) activated inflammatory CD4+ T effector (Teff) cells to brain endothelial cells under shear stress. PF-04957325 46-57 myelin oligodendrocyte glycoprotein Mus musculus 89-124 28851628-5 2017 The highly PDE8-selective enzymatic inhibitor PF-04957325 suppresses adhesion of in vivo myelin oligodendrocyte glycoprotein (MOG) activated inflammatory CD4+ T effector (Teff) cells to brain endothelial cells under shear stress. PF-04957325 46-57 myelin oligodendrocyte glycoprotein Mus musculus 126-129 28828577-1 2017 In this study, we investigated the uptake of malondialdehyde (MDA)-modified myelin oligodendrocyte glycoprotein (MOG) in the context of lipid peroxidation and its implications in CNS autoimmunity. Malondialdehyde 45-60 myelin oligodendrocyte glycoprotein Mus musculus 76-111 28828577-1 2017 In this study, we investigated the uptake of malondialdehyde (MDA)-modified myelin oligodendrocyte glycoprotein (MOG) in the context of lipid peroxidation and its implications in CNS autoimmunity. Malondialdehyde 45-60 myelin oligodendrocyte glycoprotein Mus musculus 113-116 28828577-1 2017 In this study, we investigated the uptake of malondialdehyde (MDA)-modified myelin oligodendrocyte glycoprotein (MOG) in the context of lipid peroxidation and its implications in CNS autoimmunity. Malondialdehyde 62-65 myelin oligodendrocyte glycoprotein Mus musculus 76-111 28828577-1 2017 In this study, we investigated the uptake of malondialdehyde (MDA)-modified myelin oligodendrocyte glycoprotein (MOG) in the context of lipid peroxidation and its implications in CNS autoimmunity. Malondialdehyde 62-65 myelin oligodendrocyte glycoprotein Mus musculus 113-116 27447115-4 2016 Unexpectedly, we found that spermidine treatment of MOG-specific T cells did not affect their pathogenic potency upon adaptive transfer; however, spermidine diminished the ability of macrophages in activating MOG-specific T cells ex vivo. Spermidine 28-38 myelin oligodendrocyte glycoprotein Mus musculus 52-55 29163764-5 2017 Moreover, MOG-reactive CD4+ T cells expanded in the presence of ketamine produced reduced amounts of Th17 cytokines, leading to diminished EAE severity when transferred into TCRbeta-deficient mice in comparison to those treated with vehicle. Ketamine 64-72 myelin oligodendrocyte glycoprotein Mus musculus 10-13 28011088-2 2017 We here report that nitration of tyrosine 40 in Myelin Oligodendrocyte Glycoprotein (MOG) abrogates its encephalitogenicity both at protein and peptide levels in the experimental autoimmune encephalomyelitis (EAE) model in H2b C57BL/6 mice. Tyrosine 33-41 myelin oligodendrocyte glycoprotein Mus musculus 48-83 28011088-2 2017 We here report that nitration of tyrosine 40 in Myelin Oligodendrocyte Glycoprotein (MOG) abrogates its encephalitogenicity both at protein and peptide levels in the experimental autoimmune encephalomyelitis (EAE) model in H2b C57BL/6 mice. Tyrosine 33-41 myelin oligodendrocyte glycoprotein Mus musculus 85-88 27447115-4 2016 Unexpectedly, we found that spermidine treatment of MOG-specific T cells did not affect their pathogenic potency upon adaptive transfer; however, spermidine diminished the ability of macrophages in activating MOG-specific T cells ex vivo. Spermidine 146-156 myelin oligodendrocyte glycoprotein Mus musculus 209-212 27321391-2 2016 We described that Candida albicans (Ca) aggravates experimental autoimmune encephalomyelitis (EAE) that is a model to study MS. We also observed that vaccination with a myelin peptide (MOG) in the presence of vitamin D (VitD) protected mice against EAE. Vitamin D 209-218 myelin oligodendrocyte glycoprotein Mus musculus 185-188 27619998-6 2016 IFN-beta + NAg in Alum vaccination elicited elevated numbers and percentages of FOXP3+ T cells in blood and secondary lymphoid organs in 2D2 MOG-specific transgenic mice, and repeated boosters facilitated generation of activated CD44high CD25+ regulatory T cell (Treg) populations. nag 11-14 myelin oligodendrocyte glycoprotein Mus musculus 141-144 26735612-3 2016 We demonstrated that melatonin exhibits a therapeutic role by ameliorating the clinical severity and restricting the infiltration of inflammatory Th17 cells into the CNS of mice with myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Melatonin 21-30 myelin oligodendrocyte glycoprotein Mus musculus 183-218 27403263-5 2016 EAE was induced with myelin oligodendrocyte glycoprotein (MOG), and one group was treated with AT, at a dose of 100 mg/kg on the 3(th) day post-immunization with MOG, the other group was treated with 1% alcohol. alpha-Tocopherol 95-97 myelin oligodendrocyte glycoprotein Mus musculus 162-165 27381476-6 2016 In the cuprizone-fed mouse model of demyelination, ODC derived demethylated MOG cfDNA was increased in serum and was associated with tissue-wide demyelination, demonstrating the utility of demethylated MOG cfDNA as a biomarker of ODC death. Cuprizone 7-16 myelin oligodendrocyte glycoprotein Mus musculus 76-79 27381476-6 2016 In the cuprizone-fed mouse model of demyelination, ODC derived demethylated MOG cfDNA was increased in serum and was associated with tissue-wide demyelination, demonstrating the utility of demethylated MOG cfDNA as a biomarker of ODC death. Cuprizone 7-16 myelin oligodendrocyte glycoprotein Mus musculus 202-205 27256343-1 2016 BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. Cannabinoids 66-77 myelin oligodendrocyte glycoprotein Mus musculus 141-176 27256343-1 2016 BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. Cannabidiol 79-90 myelin oligodendrocyte glycoprotein Mus musculus 141-176 27256343-1 2016 BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. Cannabidiol 79-90 myelin oligodendrocyte glycoprotein Mus musculus 178-181 27256343-1 2016 BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. Cannabidiol 92-95 myelin oligodendrocyte glycoprotein Mus musculus 141-176 27256343-1 2016 BACKGROUND: Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. Cannabidiol 92-95 myelin oligodendrocyte glycoprotein Mus musculus 178-181 26822306-8 2016 Thus, the goal of this work was to investigate the modulation of MOG-specific immune responses with subchronic low dose TCDD (0.1-1.0 mug/kg/d for 12 days) in EAE without PTX. Polychlorinated Dibenzodioxins 120-124 myelin oligodendrocyte glycoprotein Mus musculus 65-68 26822306-9 2016 The results demonstrate that subchronic, low dose exposure of TCDD attenuates the immune responses in EAE development in the absence of PTX, which is due in part to suppression of MOG-specific IL-17A and IFN-gamma responses. Polychlorinated Dibenzodioxins 62-66 myelin oligodendrocyte glycoprotein Mus musculus 180-183 25579380-8 2016 Interestingly, onset and posttreatment with BVA at the ST36 acupoint markedly attenuated neurological impairment in myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE mice compared to treatment with BVA at six placebo acupoints. Trihydroxy[(N-Hydroxybenzamidato)oxo]vanadate 44-47 myelin oligodendrocyte glycoprotein Mus musculus 116-151 25579380-8 2016 Interestingly, onset and posttreatment with BVA at the ST36 acupoint markedly attenuated neurological impairment in myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE mice compared to treatment with BVA at six placebo acupoints. Trihydroxy[(N-Hydroxybenzamidato)oxo]vanadate 44-47 myelin oligodendrocyte glycoprotein Mus musculus 153-156 25579380-8 2016 Interestingly, onset and posttreatment with BVA at the ST36 acupoint markedly attenuated neurological impairment in myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE mice compared to treatment with BVA at six placebo acupoints. Trihydroxy[(N-Hydroxybenzamidato)oxo]vanadate 217-220 myelin oligodendrocyte glycoprotein Mus musculus 153-156 26943953-2 2016 We treated C57Bl/6 mice with MOG--induced EAE daily with DHF starting on the day of disease induction. 6,7-dihydroxyflavone 57-60 myelin oligodendrocyte glycoprotein Mus musculus 29-32 26762804-3 2016 We recently described the therapeutic activity of the association between myelin oligodendrocyte glycoprotein peptide (MOG) and active vitamin D3 (VitD) against experimental autoimmune encephalomyelitis (EAE). Cholecalciferol 135-145 myelin oligodendrocyte glycoprotein Mus musculus 74-117 26735612-3 2016 We demonstrated that melatonin exhibits a therapeutic role by ameliorating the clinical severity and restricting the infiltration of inflammatory Th17 cells into the CNS of mice with myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Melatonin 21-30 myelin oligodendrocyte glycoprotein Mus musculus 220-223 26075905-3 2015 Utilizing mice deficient in cysteine cathepsins both individually and in combination, we found that the myelin-associated antigen myelin oligodendrocyte glycoprotein (MOG) was efficiently processed and presented by macrophages to CD4+ T cells in the individual absence of cathepsin B, S or L. Similarly, mice deficient in cathepsin B or S were susceptible to MOG-induced EAE and displayed clinical progression and immune infiltration into the CNS, similar to their wild-type counterparts. Cysteine 28-36 myelin oligodendrocyte glycoprotein Mus musculus 167-170 27764518-0 2016 Administration of vitamin D3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination. Cholecalciferol 18-28 myelin oligodendrocyte glycoprotein Mus musculus 48-83 27764518-0 2016 Administration of vitamin D3 induces CNPase and myelin oligodendrocyte glycoprotein expression in the cerebral cortex of the murine model of cuprizone-induced demyelination. Cuprizone 141-150 myelin oligodendrocyte glycoprotein Mus musculus 48-83 27764518-11 2016 However, a significant increase in the MOG and CNPase expression was seen in vitamin D injected group as compared to SHAM and control groups. Vitamin D 77-86 myelin oligodendrocyte glycoprotein Mus musculus 39-42 27764518-12 2016 It is concluded that vitamin D plays a role in the process of remyelination by increasing MOG and CNPase expression in the cortex. Vitamin D 21-30 myelin oligodendrocyte glycoprotein Mus musculus 90-93 26130320-4 2015 Melatonin was tested for its effect on Th1, Th17 and T regulatory (Treg) cells in the lymph nodes and CNS of immunodominant peptide of myelin oligodendrocyte glycoprotein (pMOG)-immunized and EAE mice, respectively. Melatonin 0-9 myelin oligodendrocyte glycoprotein Mus musculus 135-170 25637488-10 2015 However, there is an antagonistic interaction between CBD and PEA in protection against MOG-induced disease. Cannabidiol 54-57 myelin oligodendrocyte glycoprotein Mus musculus 88-91 25965341-2 2015 Considering the tolerogenic effects of active vitamin D, we evaluated the therapeutic effect of myelin oligodendrocyte glycoprotein (MOG) associated with active vitamin D in EAE development. Vitamin D 161-170 myelin oligodendrocyte glycoprotein Mus musculus 96-131 25965341-2 2015 Considering the tolerogenic effects of active vitamin D, we evaluated the therapeutic effect of myelin oligodendrocyte glycoprotein (MOG) associated with active vitamin D in EAE development. Vitamin D 161-170 myelin oligodendrocyte glycoprotein Mus musculus 133-136 25965341-11 2015 The association of MOG with 1,25(OH)2D3 was able to control EAE development. Calcitriol 28-39 myelin oligodendrocyte glycoprotein Mus musculus 19-22 25762107-8 2015 Further in vitro studies showed that kirenol inhibited viability of MOG-specific lymphocytes and induced apoptosis of MOG-specific CD4+ T cells in a dose- and time-dependent manner. kirenol 37-44 myelin oligodendrocyte glycoprotein Mus musculus 68-71 25880134-1 2015 BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. Cannabidiol 12-23 myelin oligodendrocyte glycoprotein Mus musculus 166-201 25880134-1 2015 BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. Cannabidiol 12-23 myelin oligodendrocyte glycoprotein Mus musculus 203-206 25880134-1 2015 BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. Cannabidiol 25-28 myelin oligodendrocyte glycoprotein Mus musculus 166-201 25880134-1 2015 BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. Cannabidiol 25-28 myelin oligodendrocyte glycoprotein Mus musculus 203-206 25880134-1 2015 BACKGROUND: Cannabidiol (CBD), the main non-psychoactive cannabinoid, has been previously shown by us to ameliorate clinical symptoms and to decrease inflammation in myelin oligodendrocyte glycoprotein (MOG)35-55-induced mouse experimental autoimmune encephalomyelitis model of multiple sclerosis as well as to decrease MOG35-55-induced T cell proliferation and IL-17 secretion. Cannabinoids 57-68 myelin oligodendrocyte glycoprotein Mus musculus 166-201 25762107-6 2015 Priming of lymphocytes was reduced and apoptosis of MOG-activated CD4+ T cells was increased in kirenol treated EAE mice. kirenol 96-103 myelin oligodendrocyte glycoprotein Mus musculus 52-55 25762107-8 2015 Further in vitro studies showed that kirenol inhibited viability of MOG-specific lymphocytes and induced apoptosis of MOG-specific CD4+ T cells in a dose- and time-dependent manner. kirenol 37-44 myelin oligodendrocyte glycoprotein Mus musculus 118-121 26216117-4 2015 The aim of this study was to demonstrate the role of LIF on Opalin and myelin oligodendrocyte glycoprotein (MOG) expression in the cerebral cortex of cuprizone-induced MS mice. Cuprizone 150-159 myelin oligodendrocyte glycoprotein Mus musculus 71-106 26216117-4 2015 The aim of this study was to demonstrate the role of LIF on Opalin and myelin oligodendrocyte glycoprotein (MOG) expression in the cerebral cortex of cuprizone-induced MS mice. Cuprizone 150-159 myelin oligodendrocyte glycoprotein Mus musculus 108-111 24433027-3 2014 In this study, we show treatment of experimental autoimmune encephalomyelitis (EAE), a model of MS, by coencapsulating the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) with dexamethasone (DXM) into acetalated dextran (Ac-DEX) microparticles (DXM/MOG/MPs) and administering the microparticles subcutaneously. ac-dex 241-247 myelin oligodendrocyte glycoprotein Mus musculus 149-184 25437209-6 2014 alpha-NETA significantly delayed the onset of EAE induced in C57BL/6 mice by both active immunization with myelin oligodendrocyte glycoprotein peptide 35-55 and by adoptive transfer of encephalitogenic T cells. 2-naphthoylethyltrimethylammonium 0-10 myelin oligodendrocyte glycoprotein Mus musculus 107-142 25242632-2 2014 In mice immunized with myelin oligodendrocyte glycoprotein peptide, the BBB-permeable COMT inhibitor dinitrocatechol (DNC) reduced clinical signs, while entacapone, a non-BBB-permeable inhibitor, had no effect. 3,4-Dinitrocatechol 101-116 myelin oligodendrocyte glycoprotein Mus musculus 23-58 25242632-2 2014 In mice immunized with myelin oligodendrocyte glycoprotein peptide, the BBB-permeable COMT inhibitor dinitrocatechol (DNC) reduced clinical signs, while entacapone, a non-BBB-permeable inhibitor, had no effect. dnc 118-121 myelin oligodendrocyte glycoprotein Mus musculus 23-58 25375337-8 2014 It was found that the substitutions of Arg at positions 41 and 46 with Ala results in peptide analogues that reduce the severity of MOG-induced EAE clinical symptoms in C57BL/6 mice when co-administered with mouse MOG35-55 peptide at the time of immunization. Arginine 39-42 myelin oligodendrocyte glycoprotein Mus musculus 132-135 25375337-8 2014 It was found that the substitutions of Arg at positions 41 and 46 with Ala results in peptide analogues that reduce the severity of MOG-induced EAE clinical symptoms in C57BL/6 mice when co-administered with mouse MOG35-55 peptide at the time of immunization. Alanine 71-74 myelin oligodendrocyte glycoprotein Mus musculus 132-135 25289890-4 2014 The MOG-CFA/PTX and CFA/PTX produced similar effects, although those caused by the former were consistently more marked. 3-chloro-4-fluoroaniline 8-11 myelin oligodendrocyte glycoprotein Mus musculus 4-7 25289890-4 2014 The MOG-CFA/PTX and CFA/PTX produced similar effects, although those caused by the former were consistently more marked. ptx 12-15 myelin oligodendrocyte glycoprotein Mus musculus 4-7 25289890-8 2014 Our results suggest that CFA/PTX primes the CP for neuroinflammation by inducing structural changes that are exacerbated when there is an immune response to MOG and reinforce the CP as a gateway for leukocytes to enter the CNS by accessing the CSF and leptomeninges. 3-chloro-4-fluoroaniline 25-28 myelin oligodendrocyte glycoprotein Mus musculus 157-160 25289890-8 2014 Our results suggest that CFA/PTX primes the CP for neuroinflammation by inducing structural changes that are exacerbated when there is an immune response to MOG and reinforce the CP as a gateway for leukocytes to enter the CNS by accessing the CSF and leptomeninges. ptx 29-32 myelin oligodendrocyte glycoprotein Mus musculus 157-160 25037177-0 2014 Glutathione PEGylated liposomal methylprednisolone (2B3-201) attenuates CNS inflammation and degeneration in murine myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis. Glutathione 0-11 myelin oligodendrocyte glycoprotein Mus musculus 116-151 25037177-0 2014 Glutathione PEGylated liposomal methylprednisolone (2B3-201) attenuates CNS inflammation and degeneration in murine myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis. Methylprednisolone 32-50 myelin oligodendrocyte glycoprotein Mus musculus 116-151 25037177-9 2014 In summary, in the murine MOG-EAE model of MS, a glutathione PEGylated liposomal formulation of MP (2B3-201) is clinically and histologically as effective as free MP at one tenth of the dosage as well as at a lower application frequency and clearly more effective than the same dosage of free MP. Glutathione 49-60 myelin oligodendrocyte glycoprotein Mus musculus 26-29 24869907-4 2014 We found that disease activity was inhibited in a myelin oligodendrocyte glycoprotein (MOG) peptide-induced EAE mouse briefly pretreated with low-dose (0.15 mg/kg) 5-Aza, ameliorating significant CNS inflammatory responses, as indicated by greatly decreased proinflammatory cytokines. Decitabine 164-169 myelin oligodendrocyte glycoprotein Mus musculus 50-85 24869907-4 2014 We found that disease activity was inhibited in a myelin oligodendrocyte glycoprotein (MOG) peptide-induced EAE mouse briefly pretreated with low-dose (0.15 mg/kg) 5-Aza, ameliorating significant CNS inflammatory responses, as indicated by greatly decreased proinflammatory cytokines. Decitabine 164-169 myelin oligodendrocyte glycoprotein Mus musculus 87-90 24799564-4 2014 DNP treatments attenuated infiltration of effector T cells into the CNS and suppressed innate and adaptive immune responses to myelin oligodendrocyte glycoprotein immunization in spleen. dnp 0-3 myelin oligodendrocyte glycoprotein Mus musculus 127-162 24471474-8 2014 Although disease incidence and severity were similar, the average day of disease onset occurred approximately 5 days earlier with the use of MOG-B-containing trifluoroacetate. Trifluoroacetic Acid 158-174 myelin oligodendrocyte glycoprotein Mus musculus 141-144 24433027-3 2014 In this study, we show treatment of experimental autoimmune encephalomyelitis (EAE), a model of MS, by coencapsulating the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) with dexamethasone (DXM) into acetalated dextran (Ac-DEX) microparticles (DXM/MOG/MPs) and administering the microparticles subcutaneously. Dexamethasone 196-209 myelin oligodendrocyte glycoprotein Mus musculus 149-184 24433027-3 2014 In this study, we show treatment of experimental autoimmune encephalomyelitis (EAE), a model of MS, by coencapsulating the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) with dexamethasone (DXM) into acetalated dextran (Ac-DEX) microparticles (DXM/MOG/MPs) and administering the microparticles subcutaneously. Dexamethasone 211-214 myelin oligodendrocyte glycoprotein Mus musculus 149-184 24433027-3 2014 In this study, we show treatment of experimental autoimmune encephalomyelitis (EAE), a model of MS, by coencapsulating the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) with dexamethasone (DXM) into acetalated dextran (Ac-DEX) microparticles (DXM/MOG/MPs) and administering the microparticles subcutaneously. acetalated dextran 221-239 myelin oligodendrocyte glycoprotein Mus musculus 149-184 26216117-0 2015 Administration of leukemia inhibitory factor increases Opalin and myelin oligodendrocyte glycoprotein expression in the cerebral cortex in a cuprizone-induced model of demyelination. Cuprizone 141-150 myelin oligodendrocyte glycoprotein Mus musculus 66-101 25019206-1 2014 Chronic treatment with caffeine, the most widely consumed psychoactive drug and a non-selective antagonist of adenosine receptors, can protection against myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Caffeine 23-31 myelin oligodendrocyte glycoprotein Mus musculus 154-189 25019206-1 2014 Chronic treatment with caffeine, the most widely consumed psychoactive drug and a non-selective antagonist of adenosine receptors, can protection against myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Caffeine 23-31 myelin oligodendrocyte glycoprotein Mus musculus 191-194 24778444-5 2014 Computational and experimental analyses indicated that the I-A(b) binding region of the immunodominant peptide of MOG is susceptible to cleavage by the NOX2-controlled cysteine cathepsins L and S in a redox-dependent manner. Cysteine 168-176 myelin oligodendrocyte glycoprotein Mus musculus 114-117 24433027-3 2014 In this study, we show treatment of experimental autoimmune encephalomyelitis (EAE), a model of MS, by coencapsulating the immunodominant peptide of myelin oligodendrocyte glycoprotein (MOG) with dexamethasone (DXM) into acetalated dextran (Ac-DEX) microparticles (DXM/MOG/MPs) and administering the microparticles subcutaneously. Dexamethasone 265-268 myelin oligodendrocyte glycoprotein Mus musculus 149-184 24433027-6 2014 Additionally, treatment with DXM/MOG/MPs significantly inhibited disease-associated cytokine (e.g., IL-17, GM-CSF) expression in splenocytes isolated in treated mice. Dexamethasone 29-32 myelin oligodendrocyte glycoprotein Mus musculus 33-36 23550596-3 2013 In this study, we found that ALA restricts the infiltration of inflammatory cells into the CNS (central nervous system) in MOG (myelin oligodendrocyte glycoprotein)-EAE mice, thus reducing the disease severity. Thioctic Acid 29-32 myelin oligodendrocyte glycoprotein Mus musculus 123-126 24323580-7 2014 AZD1480 treatment inhibits disease severity in myelin oligodendrocyte glycoprotein-induced classical and atypical EAE models by preventing entry of immune cells into the brain, suppressing differentiation of Th1 and Th17 cells, deactivating myeloid cells, inhibiting STAT activation in the brain, and reducing expression of proinflammatory cytokines and chemokines. AZD 1480 0-7 myelin oligodendrocyte glycoprotein Mus musculus 47-82 23550596-3 2013 In this study, we found that ALA restricts the infiltration of inflammatory cells into the CNS (central nervous system) in MOG (myelin oligodendrocyte glycoprotein)-EAE mice, thus reducing the disease severity. Thioctic Acid 29-32 myelin oligodendrocyte glycoprotein Mus musculus 128-163 23550596-6 2013 Together, these data suggest that ALA can up-regulate endogenous systemic and central PPAR-gamma and enhance systemic Treg-cells to inhibit the inflammatory response and ameliorate MOG-EAE. Thioctic Acid 34-37 myelin oligodendrocyte glycoprotein Mus musculus 181-184 23443463-0 2013 Ciliary neurotrophic factor role in myelin oligodendrocyte glycoprotein expression in Cuprizone-induced multiple sclerosis mice. Cuprizone 86-95 myelin oligodendrocyte glycoprotein Mus musculus 36-71 23843531-4 2013 Here, we examined the ability of TFA-12, a new synthetic compound belonging to tocopherol long-chain fatty alcohols, to promote oligodendrocyte regeneration and remyelination in experimental models of MS. We showed that TFA-12 significantly ameliorates neurological deficit and severity of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) in mice. TFA-12 33-39 myelin oligodendrocyte glycoprotein Mus musculus 290-325 23843531-4 2013 Here, we examined the ability of TFA-12, a new synthetic compound belonging to tocopherol long-chain fatty alcohols, to promote oligodendrocyte regeneration and remyelination in experimental models of MS. We showed that TFA-12 significantly ameliorates neurological deficit and severity of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) in mice. TFA-12 220-226 myelin oligodendrocyte glycoprotein Mus musculus 290-325 23840675-7 2013 METHODOLOGY: Cell culture experiments demonstrated that 670 nm light-mediated photobiomodulation attenuated antigen-specific nitric oxide production by heterogenous lymphocyte populations isolated from MOG immunized mice. Nitric Oxide 125-137 myelin oligodendrocyte glycoprotein Mus musculus 202-205 23686493-3 2013 Indeed, when Ig-myelin oligodendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administered into either T cell-sufficient or -deficient mice, only the T cell-sufficient hosts yielded CD8alpha(+) and CD8alpha(-) LP DCs that were able to transfer tolerance to a variety of MHC class II-restricted effector T cells. leucylproline 233-235 myelin oligodendrocyte glycoprotein Mus musculus 13-51 23686493-3 2013 Indeed, when Ig-myelin oligodendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administered into either T cell-sufficient or -deficient mice, only the T cell-sufficient hosts yielded CD8alpha(+) and CD8alpha(-) LP DCs that were able to transfer tolerance to a variety of MHC class II-restricted effector T cells. leucylproline 233-235 myelin oligodendrocyte glycoprotein Mus musculus 53-56 23686493-4 2013 Surprisingly, these LP DCs upregulated programmed cell death ligand 1 during the initial interaction with MOG-specific T cells and used this inhibitory molecule to suppress activation of T cells regardless of Ag specificity. leucylproline 20-22 myelin oligodendrocyte glycoprotein Mus musculus 106-109 23360710-0 2013 Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model. Copper 0-6 myelin oligodendrocyte glycoprotein Mus musculus 112-115 23360710-0 2013 Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model. Clioquinol 25-35 myelin oligodendrocyte glycoprotein Mus musculus 112-115 23443463-3 2013 The aim of this study was to demonstrate the role of CNTF on MOG expression in the cerebral cortex of Cuprizone-induced MS mice. Cuprizone 102-111 myelin oligodendrocyte glycoprotein Mus musculus 61-64 22586035-3 2012 We undertook the present studies to determine if GILT(-/-) mice would process exogenously administered myelin oligodendrocyte glycoprotein (MOG), which contains disulfide bonds, to generate experimental autoimmune encephalomyelitis (EAE) to the endogenous protein. Disulfides 161-170 myelin oligodendrocyte glycoprotein Mus musculus 103-138 22694476-5 2012 In this study, treosulfan was used as a nonmyeloablative agent to generate BM chimeras encoding MOG and assessed in models of EAE induction and reversal. treosulfan 15-25 myelin oligodendrocyte glycoprotein Mus musculus 96-99 23294897-0 2013 Copper-zinc superoxide dismutase-deficient mice show increased susceptibility to experimental autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein 35-55. Copper 0-6 myelin oligodendrocyte glycoprotein Mus musculus 136-171 23194644-4 2013 GABA-treated mice showed enhanced MOG-dependent proliferation and were skewed towards a T helper 1 phenotype. gamma-Aminobutyric Acid 0-4 myelin oligodendrocyte glycoprotein Mus musculus 34-37 22586035-3 2012 We undertook the present studies to determine if GILT(-/-) mice would process exogenously administered myelin oligodendrocyte glycoprotein (MOG), which contains disulfide bonds, to generate experimental autoimmune encephalomyelitis (EAE) to the endogenous protein. Disulfides 161-170 myelin oligodendrocyte glycoprotein Mus musculus 140-143 21965673-4 2011 Here, we report that oral GlcNAc inhibits T-helper 1 (Th1) and T-helper 17 (Th17) responses and attenuates the clinical severity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE when administered after disease onset. Acetylglucosamine 26-32 myelin oligodendrocyte glycoprotein Mus musculus 132-167 21994003-4 2012 Regulatory effects of vitamin D3 treatment that were MER dependent included increased levels of IL-10 and IL-6 secreted by MOG peptide-reactive splenocytes and increased expression of CCL5, CCR1 & CCR3 in spleen tissue. Cholecalciferol 22-32 myelin oligodendrocyte glycoprotein Mus musculus 123-126 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 70-105 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 107-110 22291191-5 2012 Administration of these 5-FU-resistant CD11b(-)CD45(-) MSCs 6 d after myelin oligodendrocyte glycoprotein (MOG) immunization completely remitted MOG-induced experimental autoimmune encephalomyelitis after initial development of mild disease. Fluorouracil 24-28 myelin oligodendrocyte glycoprotein Mus musculus 145-148 21964417-5 2011 Strikingly, two doses of BBR3378 given a week after EAE induction were sufficient to provide significant protection from clinical symptoms and reduce MOG-specific proinflammatory T cell cytokine production, and serum IgG responses. BBR3378 25-32 myelin oligodendrocyte glycoprotein Mus musculus 150-153 21965673-4 2011 Here, we report that oral GlcNAc inhibits T-helper 1 (Th1) and T-helper 17 (Th17) responses and attenuates the clinical severity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE when administered after disease onset. Acetylglucosamine 26-32 myelin oligodendrocyte glycoprotein Mus musculus 169-172 21965673-6 2011 Initiating oral GlcNAc treatment on the second day of clinical disease inhibited MOG-induced EAE as well as secretion of interferon-gamma, tumor necrosis factor-alpha, interleukin-17, and interleukin-22. Acetylglucosamine 16-22 myelin oligodendrocyte glycoprotein Mus musculus 81-84 21429524-4 2011 Furthermore, laquinimod minimizes inflammation, demyelination and axonal damage in MOG-induced EAE in mice treated at disease induction and following clinical disease onset. laquinimod 13-23 myelin oligodendrocyte glycoprotein Mus musculus 83-86 21237519-1 2011 We investigated the optimum doses of phenytoin for treatment of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE). Phenytoin 37-46 myelin oligodendrocyte glycoprotein Mus musculus 64-99 20399559-6 2010 We show here that female C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein (MOG(35-55)) display a significant decrease in elicited pain behaviours in response to formalin injection. Formaldehyde 176-184 myelin oligodendrocyte glycoprotein Mus musculus 53-88 21354971-5 2011 First we have studied effects of dimethylfumarate on the disease course, central nervous system, tissue integrity and the molecular mechanism of action in an animal model of chronic multiple sclerosis: myelin oligodendrocyte glycoprotein induced experimental autoimmune encephalomyelitis in C57BL/6 mice. Dimethyl Fumarate 33-49 myelin oligodendrocyte glycoprotein Mus musculus 202-237 20077431-2 2010 Here we further confirm that Fasudil, a selective Rock inhibitor, has therapeutic potential in a mouse model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE). fasudil 29-36 myelin oligodendrocyte glycoprotein Mus musculus 112-147 20077431-2 2010 Here we further confirm that Fasudil, a selective Rock inhibitor, has therapeutic potential in a mouse model of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE). fasudil 29-36 myelin oligodendrocyte glycoprotein Mus musculus 149-152 21256121-2 2011 This study examined the long term effects of the opioid growth factor (OGF, [Met(5)]-enkephalin) and a low dose of the opioid antagonist naltrexone (LDN) on expression of myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Naltrexone 137-147 myelin oligodendrocyte glycoprotein Mus musculus 171-206 21256121-2 2011 This study examined the long term effects of the opioid growth factor (OGF, [Met(5)]-enkephalin) and a low dose of the opioid antagonist naltrexone (LDN) on expression of myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Naltrexone 137-147 myelin oligodendrocyte glycoprotein Mus musculus 208-211 21256121-5 2011 Both severity and disease indices of EAE in OGF- and LDN-treated mice were notably decreased from MOG+Vehicle cohorts. LDN 53-56 myelin oligodendrocyte glycoprotein Mus musculus 98-101 21297130-4 2011 In C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein peptide 35-55 to develop chronic disease, cortical and spinal cord levels of noradrenaline were significantly reduced versus control mice. Norepinephrine 144-157 myelin oligodendrocyte glycoprotein Mus musculus 31-66 20955831-5 2011 Therapeutic administration of FTY720 (0.03 to 1 mg/kg) significantly improved the symptoms of chronic EAE induced by myelin oligodendrocyte glycoprotein in C57BL/6 mice whereas rm-IFN-beta (10,000 IU/mouse) showed no clear effect. Fingolimod Hydrochloride 30-36 myelin oligodendrocyte glycoprotein Mus musculus 117-152 20399559-6 2010 We show here that female C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein (MOG(35-55)) display a significant decrease in elicited pain behaviours in response to formalin injection. Formaldehyde 176-184 myelin oligodendrocyte glycoprotein Mus musculus 90-93 19965930-3 2010 CpdA treatment of mice, both early and at the peak of the disease, markedly suppressed the clinical symptoms of EAE induced by myelin oligodendrocyte glycoprotein peptide immunization. CPDA 0-4 myelin oligodendrocyte glycoprotein Mus musculus 127-162 19965930-5 2010 In vivo CpdA therapy suppressed the encephalogenicity of myelin oligodendrocyte glycoprotein peptide-specific T cells. CPDA 8-12 myelin oligodendrocyte glycoprotein Mus musculus 57-92 19659692-7 2009 4-phenylbutyrate treatment increases expression of ACOX1, l-peroxisomal bifunctional enzyme, PLP, myelin oligodendrocyte glycoprotein, and CNPase, mainly in 158N cells. 4-phenylbutyric acid 0-16 myelin oligodendrocyte glycoprotein Mus musculus 98-133 19879252-2 2010 Caffeine, a non-selective antagonist of adenosine receptors, has been shown to provide protection against myelin oligodendroglia glycoprotein (MOG)-induced EAE in mice. Caffeine 0-8 myelin oligodendrocyte glycoprotein Mus musculus 106-141 19879252-2 2010 Caffeine, a non-selective antagonist of adenosine receptors, has been shown to provide protection against myelin oligodendroglia glycoprotein (MOG)-induced EAE in mice. Caffeine 0-8 myelin oligodendrocyte glycoprotein Mus musculus 143-146 19879259-6 2010 B cells from GA-treated mice also diminished proliferation of myelin oligodendrocyte glycoprotein (MOG(35-55)) specific T cells. Glatiramer Acetate 13-15 myelin oligodendrocyte glycoprotein Mus musculus 62-97 19879259-6 2010 B cells from GA-treated mice also diminished proliferation of myelin oligodendrocyte glycoprotein (MOG(35-55)) specific T cells. Glatiramer Acetate 13-15 myelin oligodendrocyte glycoprotein Mus musculus 99-102 19855075-5 2009 Over 33% of the MOG-treated animals receiving LDN did not exhibit behavioral signs of disease, and the severity and disease index of the LDN-treated mice were markedly reduced from cohorts injected with vehicle. LDN 46-49 myelin oligodendrocyte glycoprotein Mus musculus 16-19 19855075-5 2009 Over 33% of the MOG-treated animals receiving LDN did not exhibit behavioral signs of disease, and the severity and disease index of the LDN-treated mice were markedly reduced from cohorts injected with vehicle. LDN 137-140 myelin oligodendrocyte glycoprotein Mus musculus 16-19 19654226-7 2009 Moreover, in paclitaxel-treated, MOG-immunized mice, there was a complete inhibition of the recruitment of myeloid cells (especially macrophages) to the peripheral lymphoid organs. Paclitaxel 13-23 myelin oligodendrocyte glycoprotein Mus musculus 33-36 19188909-4 2009 Here we show that systemic anaphylaxis to the self-antigen myelin oligodendrocyte glycoprotein (MOG) 35-55 can occur in mice lacking mast cells (Kit(W)/Kit(W-v) mice) or histamine (histidine decarboxylase-deficient mice), but is prevented in mice lacking IL-4. Histamine 170-179 myelin oligodendrocyte glycoprotein Mus musculus 59-94 19286483-2 2009 We have previously reported that immunization with MOG 35-55 prior to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced injury of the dopaminergic system promotes less dopamine depletion and less dopaminergic damage of neurons in mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 70-114 myelin oligodendrocyte glycoprotein Mus musculus 51-54 19286483-2 2009 We have previously reported that immunization with MOG 35-55 prior to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced injury of the dopaminergic system promotes less dopamine depletion and less dopaminergic damage of neurons in mice. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 116-120 myelin oligodendrocyte glycoprotein Mus musculus 51-54 19286483-2 2009 We have previously reported that immunization with MOG 35-55 prior to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced injury of the dopaminergic system promotes less dopamine depletion and less dopaminergic damage of neurons in mice. Dopamine 144-152 myelin oligodendrocyte glycoprotein Mus musculus 51-54 19188909-4 2009 Here we show that systemic anaphylaxis to the self-antigen myelin oligodendrocyte glycoprotein (MOG) 35-55 can occur in mice lacking mast cells (Kit(W)/Kit(W-v) mice) or histamine (histidine decarboxylase-deficient mice), but is prevented in mice lacking IL-4. Histamine 170-179 myelin oligodendrocyte glycoprotein Mus musculus 96-99 19188909-6 2009 Thus, anaphylactic reactions to self-MOG can occur in the absence of mast cells or histamine, key elements of the classical IgE-, mast cell-, and histamine-dependent pathway of anaphylaxis. Histamine 146-155 myelin oligodendrocyte glycoprotein Mus musculus 37-40 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. beta-Lactams 106-117 myelin oligodendrocyte glycoprotein Mus musculus 194-229 19257986-11 2009 After the intervention of Tri, the levels of IL-10 were increased (P<0.05), but the secretion of INF-gamma and proliferation response of splenic lymphocytes induced by MOG(35-55); were statistically significantly inhibited(P<0.05 and P<0.01, respectively). triptolide 26-29 myelin oligodendrocyte glycoprotein Mus musculus 171-174 18485368-5 2008 Moreover, continuous treatment with phenytoin provides these protective actions for at least 180 days post-MOG injection. Phenytoin 36-45 myelin oligodendrocyte glycoprotein Mus musculus 107-110 18485368-6 2008 The withdrawal of phenytoin from mice inoculated with MOG, however, is accompanied by acute exacerbation of EAE, with significant mortality and infiltration of immune cells in the CNS. Phenytoin 18-27 myelin oligodendrocyte glycoprotein Mus musculus 54-57 18678605-4 2008 After 5 weeks of CR, EAE was induced by immunizing with proteolipid protein in SJL mice and with myelin oligodendrocyte glycoprotein in C57BL/6 mice. Chromium 17-19 myelin oligodendrocyte glycoprotein Mus musculus 97-132 19234156-5 2009 GMME1 administration to experimental autoimmune encephalomyelitis mice suppresses symptomatic disease and correlates with decreased levels of inflammatory cytokines including IL-17, MOG-specific Ab titers, and blockade of CD4 and CD8 T cell infiltration in spinal cords. gmme1 0-5 myelin oligodendrocyte glycoprotein Mus musculus 182-185 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. Ceftriaxone 130-141 myelin oligodendrocyte glycoprotein Mus musculus 194-229 18773080-2 2008 In order to identify pathways to dampen excitotoxic inflammatory CNS damage, we assessed the effects of a beta-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in "Myelin Oligodendrocyte Glycoprotein" (MOG)-induced EAE. Ceftriaxone 130-141 myelin oligodendrocyte glycoprotein Mus musculus 232-235 18773080-3 2008 Ceftriaxone profoundly ameliorated the clinical course of murine MOG-induced EAE both under preventive and therapeutic regimens. Ceftriaxone 0-11 myelin oligodendrocyte glycoprotein Mus musculus 65-68 17202353-2 2007 In the present study, we found the severity of EAE induced by another myelin autoantigen, myelin basic protein, was also decreased after treatment with ES-DC-TRAIL/MOG. es-dc 152-157 myelin oligodendrocyte glycoprotein Mus musculus 164-167 18303055-4 2008 When we transferred MOG-reactive T cells from GM2/GD2-/- or wild-type mice to wild-type mice, no significant differences were observed between the two groups. gm2 46-49 myelin oligodendrocyte glycoprotein Mus musculus 20-23 18303055-5 2008 In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. gm2 77-80 myelin oligodendrocyte glycoprotein Mus musculus 33-36 18303055-5 2008 In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2-/- or to wild-type mice, the onset of EAE in GM2/GD2-/- mice was delayed. gm2 130-133 myelin oligodendrocyte glycoprotein Mus musculus 33-36 17654737-4 2007 METHODS: We studied a mouse model of myelin oligodendrocyte glycoprotein-induced EAE treated with phenytoin or carbamazepine. Phenytoin 98-107 myelin oligodendrocyte glycoprotein Mus musculus 37-72 17654737-4 2007 METHODS: We studied a mouse model of myelin oligodendrocyte glycoprotein-induced EAE treated with phenytoin or carbamazepine. Carbamazepine 111-124 myelin oligodendrocyte glycoprotein Mus musculus 37-72 17523133-0 2007 Malondialdehyde modification of myelin oligodendrocyte glycoprotein leads to increased immunogenicity and encephalitogenicity. Malondialdehyde 0-15 myelin oligodendrocyte glycoprotein Mus musculus 32-67 17579036-6 2007 Treatment with the IKK2-inhibitory compound PS-1145 reduced MOG(35-55)-specific proliferation and cytokine production of 2D2 transgenic spleen cells in vitro and diminished clinical signs of EAE in vivo. PS1145 44-51 myelin oligodendrocyte glycoprotein Mus musculus 60-63 18568646-0 2008 Methylprednisolone induces reversible clinical and pathological remission and loss of lymphocyte reactivity to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis. Methylprednisolone 0-18 myelin oligodendrocyte glycoprotein Mus musculus 111-146 18568646-6 2008 Methylprednisolone remitted the clinical signs of EAE and the inflammatory infiltrate in the CNS, accompanied by loss of lymphocyte reactivity to MOG(35-55) peptide. Methylprednisolone 0-18 myelin oligodendrocyte glycoprotein Mus musculus 146-149 18568646-7 2008 Methylprednisolone withdrawal initiated relapse of the clinical features, a return of the CNS inflammatory infiltrate and lymphocyte reactivity to MOG(35-55) peptide. Methylprednisolone 0-18 myelin oligodendrocyte glycoprotein Mus musculus 147-150 17056528-6 2006 We report that vitamin D(3) and 1,25-(OH)(2)D(3) strongly inhibited myelin oligodendrocyte peptide (MOG(35-55))-induced EAE in C57BL/6 mice, but completely failed to inhibit EAE in mice with a disrupted IL-10 or IL-10R gene. Vitamin D 15-24 myelin oligodendrocyte glycoprotein Mus musculus 100-103 18320716-6 2007 As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. Dopamine 32-40 myelin oligodendrocyte glycoprotein Mus musculus 95-98 18320716-6 2007 As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. Dopamine 42-44 myelin oligodendrocyte glycoprotein Mus musculus 95-98 18320716-6 2007 As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. Serotonin 50-59 myelin oligodendrocyte glycoprotein Mus musculus 95-98 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Homovanillic Acid 13-29 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Dopamine 30-38 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Homovanillic Acid 40-43 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Dopamine 44-46 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. 3,4-Dihydroxyphenylacetic Acid 52-83 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Dopamine 84-92 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. 3,4-Dihydroxyphenylacetic Acid 94-99 myelin oligodendrocyte glycoprotein Mus musculus 136-139 18320716-7 2007 The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Dopamine 100-102 myelin oligodendrocyte glycoprotein Mus musculus 136-139 17056528-6 2006 We report that vitamin D(3) and 1,25-(OH)(2)D(3) strongly inhibited myelin oligodendrocyte peptide (MOG(35-55))-induced EAE in C57BL/6 mice, but completely failed to inhibit EAE in mice with a disrupted IL-10 or IL-10R gene. 1,25-(oh)(2 32-43 myelin oligodendrocyte glycoprotein Mus musculus 100-103 17056528-6 2006 We report that vitamin D(3) and 1,25-(OH)(2)D(3) strongly inhibited myelin oligodendrocyte peptide (MOG(35-55))-induced EAE in C57BL/6 mice, but completely failed to inhibit EAE in mice with a disrupted IL-10 or IL-10R gene. Deuterium 23-24 myelin oligodendrocyte glycoprotein Mus musculus 100-103 16914558-3 2006 In this study, we examined the effects of DZ2002 on active EAE induced by myelin oligodendrocyte glycoprotein (MOG) 35-55 in female C57BL/6 mice. methyl 4-(adenin-9-yl)-2-hydroxybutanoate 42-48 myelin oligodendrocyte glycoprotein Mus musculus 74-109 16914558-3 2006 In this study, we examined the effects of DZ2002 on active EAE induced by myelin oligodendrocyte glycoprotein (MOG) 35-55 in female C57BL/6 mice. methyl 4-(adenin-9-yl)-2-hydroxybutanoate 42-48 myelin oligodendrocyte glycoprotein Mus musculus 111-114 16835249-5 2006 Celecoxib, but not other COX-2 inhibitors such as nimesulid, prevented myelin oligodendrocyte glycoprotein (MOG) induced EAE when administrated orally on the day of disease induction. Celecoxib 0-9 myelin oligodendrocyte glycoprotein Mus musculus 71-106 16835249-5 2006 Celecoxib, but not other COX-2 inhibitors such as nimesulid, prevented myelin oligodendrocyte glycoprotein (MOG) induced EAE when administrated orally on the day of disease induction. Celecoxib 0-9 myelin oligodendrocyte glycoprotein Mus musculus 108-111 16835249-7 2006 In celecoxib-treated mice, interferon-gamma (IFN-gamma) production from MOG-specific T cells was reduced and MOG-specific IgG1 was elevated compared with vehicle-treated mice. Celecoxib 3-12 myelin oligodendrocyte glycoprotein Mus musculus 72-75 16835249-7 2006 In celecoxib-treated mice, interferon-gamma (IFN-gamma) production from MOG-specific T cells was reduced and MOG-specific IgG1 was elevated compared with vehicle-treated mice. Celecoxib 3-12 myelin oligodendrocyte glycoprotein Mus musculus 109-112