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Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways

BACKGROUND: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. METHODS: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanis...

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Autores principales: Lee, Min Jung, Chang, Byung Joon, Oh, Seikwan, Nah, Seung-Yeol, Cho, Ik-Hyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6187097/
https://www.ncbi.nlm.nih.gov/pubmed/30337803
http://dx.doi.org/10.1016/j.jgr.2017.04.013
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author Lee, Min Jung
Chang, Byung Joon
Oh, Seikwan
Nah, Seung-Yeol
Cho, Ik-Hyun
author_facet Lee, Min Jung
Chang, Byung Joon
Oh, Seikwan
Nah, Seung-Yeol
Cho, Ik-Hyun
author_sort Lee, Min Jung
collection PubMed
description BACKGROUND: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. METHODS: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. RESULTS: Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein (MBP)(68–82) peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-γ, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor β1, transforming growth factor β, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways in microglia/macrophages, T cells, and astrocytes. CONCLUSION: Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinase/nuclear factor-κB signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed.
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spelling pubmed-61870972018-10-18 Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways Lee, Min Jung Chang, Byung Joon Oh, Seikwan Nah, Seung-Yeol Cho, Ik-Hyun J Ginseng Res Research Article BACKGROUND: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. METHODS: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. RESULTS: Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein (MBP)(68–82) peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-γ, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor β1, transforming growth factor β, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways in microglia/macrophages, T cells, and astrocytes. CONCLUSION: Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinase/nuclear factor-κB signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed. Elsevier 2018-10 2017-05-08 /pmc/articles/PMC6187097/ /pubmed/30337803 http://dx.doi.org/10.1016/j.jgr.2017.04.013 Text en © 2017 The Korean Society of Ginseng, Published by Elsevier Korea LLC. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Lee, Min Jung
Chang, Byung Joon
Oh, Seikwan
Nah, Seung-Yeol
Cho, Ik-Hyun
Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title_full Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title_fullStr Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title_full_unstemmed Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title_short Korean Red Ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κB signaling pathways
title_sort korean red ginseng mitigates spinal demyelination in a model of acute multiple sclerosis by downregulating p38 mitogen-activated protein kinase and nuclear factor-κb signaling pathways
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6187097/
https://www.ncbi.nlm.nih.gov/pubmed/30337803
http://dx.doi.org/10.1016/j.jgr.2017.04.013
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