The inhibitory effects of Aster yomena extract on microglial activation-mediated inflammatory response and pain by modulation of the NF-κB and MAPK signaling pathways

Abstract

• Aster yomena extract (AYE) inhibited LPS-induced microglial activation in BV2 cells. • LPS-induced NF-κB and MAPK signaling pathways were inhibited via treatment of AYE. • CFA-induced inflammatory pain were alleviated by oral administration of AYE in mouse. • Chlorogenic acid and t-Ferulic acid were identified as the major active components. This study investigated the inhibitory effect and underlying mechanisms of Aster yomena extract (AYE) on microglial activation-mediated inflammatory pain. Lipopolysaccharide (LPS)-induced microglial activation exhibited increased expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines. LPS-induced microglial activation was suppressed by AYE treatment via inhibition of the NF-κB and MAPK signaling pathways. To investigate the protective effects of AYE on inflammatory pain, complete Freund’s adjuvant (CFA) was injected into the right paw of mice. Pain hypersensitivity and microglial activation in the spinal cord were markedly alleviated by oral administration of AYE. HPLC was performed and identified chlorogenic acid (CGA) and t-Ferulic acid (FRA) as the major active components in AYE. Both components showed inhibitory effects on LPS-induced microglial activation in BV2 cells. Our study demonstrates that AYE inhibits microglial activation-mediated inflammatory pain and that AYE has potential application as a natural analgesic.