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Nordihydroguaiaretic acid can suppress progression of experimental autoimmune encephalomyelitis.

08:00 EDT 10th April 2018 | BioPortfolio

Summary of "Nordihydroguaiaretic acid can suppress progression of experimental autoimmune encephalomyelitis."

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, 2018.

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Name: IUBMB life
ISSN: 1521-6551
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Experimental animal models for human AUTOIMMUNE DISEASES OF THE NERVOUS SYSTEM. They include GUILLAIN-BARRE SYNDROME (see NEURITIS, AUTOIMMUNE, EXPERIMENTAL); MYASTHENIA GRAVIS (see MYASTHENIA GRAVIS, AUTOIMMUNE, EXPERIMENTAL); and MULTIPLE SCLEROSIS (see ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL).

An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)

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