Nordihydroguaiaretic acid can suppress progression of experimental autoimmune encephalomyelitis.

Abstract

Multiple sclerosis (MS) is a poorly understood disease mechanistically. MOG35-55 peptide induced experimental autoimmune encephalomyelitis (EAE) is a broadly used model to study MS. Using this model we have earlier shown that the antioxidant tempol or the small molecule inhibitor of p38 SB203580 can effectively prevent EAE progression. This effect was mediated by means of regulating immune inflammation, signaling by the p38MAPK-SGK1 pathway, and oxidative stress. However, there is a need to test drugs that can be used in pharmacological intervention of EAE. Given that nordihydroguaiaretic Acid (NDGA) has been shown to possess anti-oxidant activity and capacity of antagonizing autoimmune inflammation, we tested the effect of NDGA in ameliorating EAE in the current study. NDGA showed significant beneficial effect against EAE with both anti-inflammation and antioxidant activity. NDGA could weaken the immune inflammation at least partly by inhibiting the oxidant stress-p38MAPK-SGK1 pathway representing a target for putative pharmacological intervention. © 2018 IUBMB Life, 70(5):432-436, 2018.

• Authors: Liang Wang, Lin Li, Mo-Yuan Quan, Dong Wang, Zhen Jia, Zhen-Fei Li, Bin Li, Li Guo, Guo-Jun Tan
• Journal: IUBMB life (IUBMB Life) Vol. 70 Issue 5 Pg. 432-436 (05 2018) ISSN: 1521-6551 [Electronic] England
• PMID: 29637686 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2018 International Union of Biochemistry and Molecular Biology.

Chemical References

• Immediate-Early Proteins
• Immunologic Factors
• Myelin-Oligodendrocyte Glycoprotein
• Neuroprotective Agents
• Peptide Fragments
• myelin oligodendrocyte glycoprotein (35-55)
• Masoprocol
• Heme Oxygenase-1
• Protein Serine-Threonine Kinases
• serum-glucocorticoid regulated kinase
• p38 Mitogen-Activated Protein Kinases

Topics

• Animals
• Demyelinating Diseases (chemically induced, drug therapy, genetics, immunology)
• Disease Progression
• Encephalomyelitis, Autoimmune, Experimental (chemically induced, drug therapy, genetics, immunology)
• Female
• Gene Expression Regulation
• Heme Oxygenase-1 (genetics, metabolism)
• Immediate-Early Proteins (antagonists & inhibitors, genetics, metabolism)
• Immunologic Factors (pharmacology)
• Injections, Intraperitoneal
• Masoprocol (pharmacology)
• Mice
• Mice, Inbred C57BL
• Myelin-Oligodendrocyte Glycoprotein
• Neuroprotective Agents (pharmacology)
• Oxidation-Reduction
• Oxidative Stress (drug effects)
• Peptide Fragments
• Protein Serine-Threonine Kinases (antagonists & inhibitors, genetics, metabolism)
• p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors, genetics, metabolism)