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

- BISA inhibits the phenotypic and functional activation of DCs.
- BISA prevents the phosphorylation of p38, JNK, and ERK in LPS-treated DCs.
- BISA reduces the nuclear translocation of NF-κB p50/p65 in LPS-treated DCs.

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.