Abstract

BackgroundThe non-saponin (NS) fraction is an important active component of Panax ginseng, with multifunctional pharmacological activities including neuroprotective, immune regulatory, anti-inflammatory, and antioxidant effects. However, the effects of NSs on multiple sclerosis (MS), a chronic and autoimmune demyelinating disorder, have not yet been demonstrated. Purposeand Methods: The goal of the present study was to demonstrate the pharmacological actions of NSs on movement dysfunctions and the related mechanisms of action using an experimental autoimmune encephalomyelitis (EAE) mouse model of MS. ResultsNSs (p.o.) alleviated movement dysfunctions in EAE mice related to reduced demyelination in the lumbar spinal cord (LSC). NSs attenuated the recruitment of microglia (CD11b+/CD45low) and macrophages (CD11b+/CD45high) in LSCs from EAE model mice, consistent with the decreased mRNA expression levels of the main proinflammatory mediators (IL-1β, COX-2, MCP-1, MIP-1α, and RANTES). NSs blocked the migration of Th17 cells (CD4+/IL17A+) and mRNA expression levels of IL-17A (product of Th17 cells) in LSCs from EAE mice. NSs suppressed alterations in blood-brain barrier (BBB) components, such as astrocytes and cell adhesion molecules, associated with inhibiting NF-κB and p38 MAPK pathways in LSCs of EAE mice and lipopolysaccharide-induced bEND.3 cells. ConclusionsNSs could attenuate movement dysfunctions and related pathological/inflammatory changes by reducing BBB permeability through NF-κB and p38 MAPK pathway inhibition in LSCs of EAE model mice. These are the first results suggesting that NSs can be potential therapeutic agents for MS by reducing BBB permeability.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.