Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome
Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Xin [verfasserIn] Li, Bin [verfasserIn] Liu, Lan [verfasserIn] Zhang, Li [verfasserIn] Ma, Tianzhao [verfasserIn] Guo, Li [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: International immunopharmacology - Amsterdam [u.a.] : Elsevier Science, 2001, 90 |
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| Übergeordnetes Werk: |
volume:90 |
| DOI / URN: |
10.1016/j.intimp.2020.107092 |
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| Katalog-ID: |
ELV005361931 |
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| 245 | 1 | 0 | |a Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
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| 520 | |a Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. | ||
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10.1016/j.intimp.2020.107092 doi (DE-627)ELV005361931 (ELSEVIER)S1567-5769(20)32764-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Wang, Xin verfasserin aut Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ Li, Bin verfasserin aut Liu, Lan verfasserin aut Zhang, Li verfasserin aut Ma, Tianzhao verfasserin aut Guo, Li verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 90 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:90 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 90 |
| spelling |
10.1016/j.intimp.2020.107092 doi (DE-627)ELV005361931 (ELSEVIER)S1567-5769(20)32764-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Wang, Xin verfasserin aut Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ Li, Bin verfasserin aut Liu, Lan verfasserin aut Zhang, Li verfasserin aut Ma, Tianzhao verfasserin aut Guo, Li verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 90 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:90 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 90 |
| allfields_unstemmed |
10.1016/j.intimp.2020.107092 doi (DE-627)ELV005361931 (ELSEVIER)S1567-5769(20)32764-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Wang, Xin verfasserin aut Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ Li, Bin verfasserin aut Liu, Lan verfasserin aut Zhang, Li verfasserin aut Ma, Tianzhao verfasserin aut Guo, Li verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 90 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:90 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 90 |
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10.1016/j.intimp.2020.107092 doi (DE-627)ELV005361931 (ELSEVIER)S1567-5769(20)32764-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Wang, Xin verfasserin aut Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ Li, Bin verfasserin aut Liu, Lan verfasserin aut Zhang, Li verfasserin aut Ma, Tianzhao verfasserin aut Guo, Li verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 90 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:90 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 90 |
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10.1016/j.intimp.2020.107092 doi (DE-627)ELV005361931 (ELSEVIER)S1567-5769(20)32764-8 DE-627 ger DE-627 rda eng 610 DE-600 PHARM DE-84 fid 44.38 bkl Wang, Xin verfasserin aut Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome 2020 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ Li, Bin verfasserin aut Liu, Lan verfasserin aut Zhang, Li verfasserin aut Ma, Tianzhao verfasserin aut Guo, Li verfasserin aut Enthalten in International immunopharmacology Amsterdam [u.a.] : Elsevier Science, 2001 90 Online-Ressource (DE-627)330614630 (DE-600)2049924-3 (DE-576)259272272 1878-1705 nnns volume:90 GBV_USEFLAG_U SYSFLAG_U GBV_ELV FID-PHARM SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.38 Pharmakologie AR 90 |
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Wang, Xin @@aut@@ Li, Bin @@aut@@ Liu, Lan @@aut@@ Zhang, Li @@aut@@ Ma, Tianzhao @@aut@@ Guo, Li @@aut@@ |
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Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. 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Wang, Xin |
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Wang, Xin ddc 610 fid PHARM bkl 44.38 misc Autophagy misc Myelin-Oligodendrocyte Glycoprotein misc Multiple sclerosis misc Inflammatory misc 3-MA misc NLRP3, NAD+ Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
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610 DE-600 PHARM DE-84 fid 44.38 bkl Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome Autophagy Myelin-Oligodendrocyte Glycoprotein Multiple sclerosis Inflammatory 3-MA NLRP3, NAD+ |
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ddc 610 fid PHARM bkl 44.38 misc Autophagy misc Myelin-Oligodendrocyte Glycoprotein misc Multiple sclerosis misc Inflammatory misc 3-MA misc NLRP3, NAD+ |
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Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
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Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
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Wang, Xin Li, Bin Liu, Lan Zhang, Li Ma, Tianzhao Guo, Li |
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nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the nlrp3 inflammasome |
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Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
| abstract |
Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. |
| abstractGer |
Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. |
| abstract_unstemmed |
Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor in numerous metabolic pathways, and so may support protective and reparative processes against central nervous system diseases such as multiple sclerosis (MS). Here, we investigated the therapeutic potential of NAD + administration in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and the contributions of autophagic regulation and NLRP3 inflammasome activity. EAE was induced in female C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein (MOG) p35-55 and disease severity analyzed by neurological function score and histological scores of spinal cord sections stained with hematoxylin–eosin or luxol fast blue. Outcomes were compared among control mice and EAE groups receiving daily post-immunization vehicle injections, NAD + injections, injection of the autophagy inhibitor 3-methyladenine (3-MA), or co-injection of NAD + and 3-MA. Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. Therefore, regulation of autophagy by NAD + treatment may be an effective therapeutic strategy for MS. |
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Nicotinamide adenine dinucleotide treatment alleviates the symptoms of experimental autoimmune encephalomyelitis by activating autophagy and inhibiting the NLRP3 inflammasome |
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Expression levels of autophagy-related proteins (Beclin1, LC3-II/I, and p62/SQSTM1) were assessed by Western blotting, the activated microglial cells were evaluated by immunohistochemistry, while mRNA expression levels of NOD-like receptor family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, IL-2, IL-17, IL-18, interferon-γ (IFN-γ) and IL-10 were detected by real-time PCR. The proportions of Th1 and Th17 cells in spleen were evaluated using flow cytometry. Treatment with NAD + alleviated demyelination, nerve injury, microglial activation and motor function abnormalities of EAE mice. In addition, NAD + increased the expressions of the autophagy-related proteins LC3-II/I and Beclin 1, and reduced the expression of p62. Treatment with NAD + also inhibited the expressions of NLRP3 and modulated the differentiation of Th1 and Th17 cells, reduced the expressions of the pro-inflammatory factors IL-1β, IL-2, IL-18, IFN-γ and IL-17, and increased the expression of anti-inflammatory IL-10. Conversely, 3-MA aggravated spinal cord inflammation and demyelination, and delayed spontaneous remission from EAE. Furthermore, the beneficial effects of NAD + were abolished by 3-MA cotreatment. Our results indicate that NAD + suppresses the NLRP3 inflammasome at least in part through the activation of autophagy to relieve the symptoms of EAE. 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| score |
7.398117 |