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

Min Jung Lee, Byung Joon Chang, Seikwan Oh, Seung Yeol Nah, Ik Hyun Cho

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)436-446
Number of pages11
JournalJournal of Ginseng Research
Volume42
Issue number4
DOIs
StatePublished - Oct 2018

Keywords

  • Korean Red Ginseng
  • demyelination
  • experimental autoimmune encephalomyelitis
  • nuclear factor-κB
  • p-38 mitogen-activated protein kinase

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