Fig. 4

Mitochondria in MS Mϕ. The upregulated glucose transporters (GLUTs) (GLUT1, GLUT3, GLUT4) and monocarboxylate transporter 1 (MCT-1) of Mϕ in patients with MS enhance glycolysis. lactate dehydrogenase A (LDHA)and MCT-4 accumulation in Mϕ also lead to increased lactate production. The 3-dihydroxy-6-methyl-7-(phenylmethyl)-4-propylnaphthalene-1-carboxylic acid (FX11) as well as α-cyano-4-hydroxy-cinnamic acid (CHCA) can reduce lactate production and inflammatory activity. Fibrin induces an increase in p47phox leading to upregulate production of ROS. This is accompanied by elevated release of iron, resulting in axonal degeneration, demyelination and mitochondrial damage. Treatment with DMF or FhHDM-1 can inhibit glycolysis and enhance oxidative phosphorylation (OXPHOS), bringing about decreasing antigen-presenting function and inflammatory mediators such as ROS, IL-6, et al. in MS Mϕ