ZFIN ID: ZDB-PUB-151110-6
Promotion of Remyelination by Sulfasalazine in a Transgenic Zebrafish Model of Demyelination
Kim, S., Lee, Y.I., Chang, K.Y., Lee, D.W., Cho, S.C., Ha, Y.W., Na, J.E., Rhyu, I.J., Park, S.C., Park, H.C.
Date: 2015
Source: Molecules and cells   38(11): 1013-21 (Journal)
Registered Authors: Kim, Suhyun, Park, Hae-Chul
Keywords: none
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Anti-Inflammatory Agents, Non-Steroidal/pharmacology*
  • Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
  • Axons/metabolism*
  • Disease Models, Animal
  • Humans
  • Immunosuppressive Agents/pharmacology*
  • Immunosuppressive Agents/therapeutic use
  • Macrophages/drug effects
  • Microglia/drug effects
  • Microglia/physiology
  • Multiple Sclerosis/drug therapy*
  • Myelin Sheath/metabolism*
  • Oligodendroglia/cytology
  • Oligodendroglia/drug effects*
  • Oligodendroglia/physiology
  • Regeneration/drug effects
  • Sulfasalazine/pharmacology
  • Sulfasalazine/therapeutic use*
  • Zebrafish
PubMed: 26549504 Full text @ Mol. Cells
Most of the axons in the vertebrate nervous system are surrounded by a lipid-rich membrane called myelin, which promotes rapid conduction of nerve impulses and protects the axon from being damaged. Multiple sclerosis (MS) is a chronic demyelinating disease of the CNS characterized by infiltration of immune cells and progressive damage to myelin and axons. One potential way to treat MS is to enhance the endogenous remyelination process, but at present there are no available treatments to promote remyelination in patients with demyelinating diseases. Sulfasalazine is an anti-inflammatory and immunemodulating drug that is used in rheumatology and inflammatory bowel disease. Its anti-inflammatory and immunomodulatory properties prompted us to test the ability of sulfasalazine to promote remyelination. In this study, we found that sulfasalazine promotes remyelination in the CNS of a transgenic zebrafish model of NTR/MTZ-induced demyelination. We also found that sulfasalazine treatment reduced the number of macrophages/microglia in the CNS of demyelinated zebrafish larvae, suggesting that the acceleration of remyelination is mediated by the immunomodulatory function of sulfasalazine. Our data suggest that temporal modulation of the immune response by sulfasalazine can be used to overcome MS by enhancing myelin repair and remyelination in the CNS.