ArticleEvidence-based complementary and alternative medicine : eCAM2022
Catalpol Regulates Oligodendrocyte Regeneration and Remyelination by Activating the GEF-Cdc42/Rac1 Signaling Pathway in EAE Mice.
Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- NG2-Glia in Central Nervous System Following Injury: From Pathological Involvement to Repair Potential.CNS neuroscience & therapeutics · 2026Review
- Catalpol: an natural multifunctional iridoid glycoside with promising therapeutic properties.Frontiers in molecular biosciences · 2026Review
- Catalpol: An Iridoid Glycoside With Potential in Combating Cancer Development and Progression-A Comprehensive Review.Phytotherapy research : PTR · 2025Review
- The Mechanisms of Mesenchymal Stem Cells in the Treatment of Experimental Autoimmune Encephalomyelitis.Current stem cell research & therapy · 2025Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main obstacle to remyelination in demyelinating diseases, such as multiple sclerosis, is the inability of oligodendrocyte precursor cells (OPCs) to differentiate into mature oligodendrocytes (OLs) in the demyelinating region. Consequently, promoting OL differentiation and myelin remodeling is a key goal in the search for treatments. Rho GTPases play diverse and important roles throughout the development of neuronal axons and the formation of the myelin sheath. The current study aimed to investigate the direct protective effects of catalpol on demyelination damage induced by myelin oligodendrocyte glycoprotein (MOG) immunization and to explore whether the GEF-Cdc42/Rac1 signaling pathway contributes to the regeneration effect induced by catalpol. In the MOG-induced experimental autoimmune encephalomyelitis (EAE) mouse model of demyelination, we observed that catalpol significantly promoted OL development by enhancing the expression of glutathione S-transferase pi (GST-pi) in the affected brain. By Luxol fast blue staining and myelin basic protein (MBP) expression assessment, catalpol was found to increase MBP expression and promote myelin repair. Furthermore, catalpol promoted OL differentiation associated with the upregulation of Cdc42/Rac1 expression and activation in vivo. In addition, PAK1/MRCK
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Registered trials
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