D. Zhu and M. Liu contributed equally to this work.
Ginsenoside Rd ameliorates experimental autoimmune encephalomyelitis in C57BL/6 mice
Article first published online: 2 MAY 2014
© 2014 Wiley Periodicals, Inc.
Journal of Neuroscience Research
Volume 92, Issue 9, pages 1217–1226, September 2014
How to Cite
Zhu, D., Liu, M., Yang, Y., Ma, L., Jiang, Y., Zhou, L., Huang, Q., Pi, R. and Chen, X. (2014), Ginsenoside Rd ameliorates experimental autoimmune encephalomyelitis in C57BL/6 mice. J. Neurosci. Res., 92: 1217–1226. doi: 10.1002/jnr.23397
- Issue published online: 12 JUL 2014
- Article first published online: 2 MAY 2014
- Manuscript Accepted: 1 APR 2014
- Manuscript Revised: 26 FEB 2014
- Manuscript Received: 28 NOV 2013
- National Natural Science Foundation of China . Grant Number: 81071068 (to X.C.).
- ginsenoside Rd;
- experimental autoimmune encephalomyelitis;
- multiple sclerosis
Multiple sclerosis (MS) is a common disabling autoimmune disease without an effective treatment in young adults. Ginsenoside Rd, extracted from Panax notoginseng, has multiple pharmacological effects and potential therapeutic applications in diseases of the central nervous system. In this study, we explore the efficacy of ginsenoside Rd in experimental autoimmune encephalomyelitis (EAE), an established model of MS. EAE was induced by myelin oligodendrocyte glycoprotein 35–55-amino-acid peptide. Ginsenoside Rd (10–80 mg/kg/day) or vehicle was intraperitoneally administered on the disease onset day, and the therapy persisted throughout the experiments. The dose of 40 mg/kg/day of ginsenoside Rd was selected as optimal. Ginsenoside Rd effectively ameliorated the clinical severity in EAE mice, reduced the permeability of the blood–brain barrier, regulated the secretion of interferon-gamma and interleukin-4, promoted the Th2 shift in vivo (cerebral cortex) and in vitro (splenocytes culture supernatants), and prevented the reduction in expression of brain-derived neurotrophic factor and nerve growth factor in both cerebral cortex and lumbar spinal cord of EAE mice. This study establishes the potency of ginsenoside Rd in inhibiting the clinical course of EAE. These findings suggest that ginsenoside Rd could be a promising agent for amelioration of neuroimmune dysfunction diseases such as MS. © 2014 Wiley Periodicals, Inc.