Microglia Polarization from M1 toward M2 Phenotype Is Promoted by Astragalus Polysaccharides Mediated through Inhibition of miR-155 in Experimental Autoimmune Encephalomyelitis

Figure 8

Schematic diagram manifesting that the balance of M1/M2 polarization phenotype in microglia via miR-155 was regulated and the A1 astrocytes were inhibited by APS in EAE. During the development of CNS inflammation and demyelination in EAE, microglia were activated first and polarized into M1 and M2 types. M1 type and M2 type were unbalanced, M1 type increased significantly, M2 type was relatively less. M1 type secreted a large number of proinflammatory factors, which on the one hand induced activation of A1 astrocytes, on the other hand to induce demyelination combined with A1 astrocytes. M2 type plays an anti-inflammatory role to inhibit demyelination. APS treatment inhibited M1 type polarization, promoted M2 type polarization, and restored the equilibrium of M1/M2 of activated microglia via miR-155. APS reduced the secretion of proinflammatory factors by M1, decreased the A1 astrocytes, and promoted the secretion of anti-inflammatory factors by M2 type, which together inhibited demyelination.