Figure 1.
Schematic diagram representing the effect of cinnamon on autoimmune demyelination. The major component of cinnamon is cinnamaldehyde, which is oxidized to cinnamic acid. This cinnamic acid then undergoes β-oxidation to be converted into benzoate that exists as sodium benzoate (NaB). In the periphery, NaB inhibits several integrins on T cells, enriches Tregs, suppresses Th17 cells, and causes Th1 to Th2 shift. On the other hand, NaB treatment leads to suppression of adhesion molecules, attenuation of mononuclear cell infiltration, decrease in proinflammatory molecules, and normalization and/or up regulation of myelin genes in the CNS compartment.