Oh, Jinhee Ha, Yujeong Kwon, Tae Woo Jo, Hyo-Sung Moon, Sang-Kwan Lee, Yoonsung Nah, Seung-Yeol Kim, Min Soo Cho, Ik-Hyun 2024-11-29T07:30:13Z 2024-11-29T07:30:13Z 2024-11-28 2025-01 1226-8453 https://pubs.kist.re.kr/handle/201004/151173 Background The 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. Purpose and 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. Results NSs (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. Conclusions NSs 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. English 고려인삼학회 Non-saponin from Panax ginseng maintains blood-brain barrier integrity by inhibiting NF-κB and p38 MAP kinase signaling pathways to prevent the progression of experimental autoimmune encephalomyelitis Article 10.1016/j.jgr.2024.09.005 1 Journal of Ginseng Research, v.49, no.1, pp.53 - 63 Journal of Ginseng Research 49 1 53 63 Y scie scopus kci 001397514400001 Plant Sciences Chemistry, Medicinal Integrative & Complementary Medicine Plant Sciences Pharmacology & Pharmacy Integrative & Complementary Medicine Article KOREAN RED GINSENG MULTIPLE-SCLEROSIS MODEL PATHOLOGY PROTEIN Non-saponin Multiple sclerosis Experimental autoimmune encephalomyelitis Blood-brain barrier Nuclear factor kappa B p38 mitogen-activated protein kinase