Bisabolangelone inhibits dendritic cell functions by blocking MAPK and NF-κB signaling

Abstract

Bisabolangelone (BISA), isolated from the roots of Angelica koreana, has many pharmacological activities, such as anti-tumor, anti-microbial, antioxidant, and anti-inflammatory activities. In this study, we investigated the anti-inflammatory mechanisms of BISA in dendritic cells (DCs), which play an essential role in innate and adaptive immune responses. BISA attenuated the production of pro-inflammatory cytokines including interleukin (IL)-12, IL-1β, and tumor necrosis factor-alpha (TNF-α), migration to macrophage inflammatory protein-3 beta, and allo-T cell activating ability of DCs. In addition, BISA affected endocytosis of DCs. Molecular studies showed that BISA suppressed MAPK phosphorylation and nuclear translocation of NF-κB p50/p65. Taken together, our data suggest that BISA inhibited DC functions by blocking MAPK and NF-κB signaling.

Keywords: BISA; Bisabolangelone; C-Jun N-terminal kinase; DCs; Dendritic cells; ERK; IκB; JNK; MAPK; MAPKs; NF-κB; bisabolangelone; dendritic cells; extracellular signal-regulated kinase; inhibits NF-κB; mitogen-activated protein kinase.