Immunoregulatory Effect of Curcumin on Experimental Autoimmune Encephalomyelitis (EAE), an Animal Model of Multiple Sclerosis (MS).

Abstract

Demyelination and progressive neurodegeneration within the central nervous system (CNS) are hallmarks of multiple sclerosis (MS), a chronic autoimmune disease. This review critically assesses the therapeutic efficacy of curcumin-a polyphenolic compound from the rhizome of Curcuma longa turmeric-in experimental autoimmune encephalomyelitis, a well-recognized animal model of MS. The significant anti-inflammatory and antioxidant properties of curcumin help slow the development of EAE. By suppressing pro-inflammatory cytokines, including interleukin-12 (IL-12), interleukin-17 (IL-17), and interferon-gamma (IFN-γ), curcumin mechanistically modifies immune responses while enhancing anti-inflammatory pathways through the upregulation of regulatory T cells (Tregs) and promotion of T helper 2 immune responses. At the same time, it enhances antiinflammatory pathways by upregulating Tregs and promoting T helper 2 (Th2) immune responses. Curcumin also has neuroprotective qualities by increasing the expression of neurotrophic factors, including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), which promote remyelination and maintain the viability of neurons. In addition, curcumin changes important intracellular signaling pathways, such as the Janus kinase/signal transducer and activator of transcription (JAK/STAT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways, which help to preserve the integrity of the blood-brain barrier (BBB) and reduce oxidative stress. Despite challenges associated with curcumin's bioavailability and pharmacokinetics, innovative delivery systems such as polymerized nano-curcumin and exosome-encapsulated formulations show promise in enhancing its therapeutic efficacy. Curcumin appears to be a promising adjunctive therapy for MS, requiring further clinical research to optimize its application in MS care.