Dieckol: an algal polyphenol attenuates urban fine dust-induced inflammation in RAW 264.7 cells via the activation of anti-inflammatory and antioxidant signaling pathways

Fine dust-associated complications related to human health are one of the major issues in the East-Asia region. In the present study, we evaluated anti-inflammatory effect of dieckol in fine dust-stimulated RAW 264.7 macrophage cells and its biological mechanism. The result showed that the exposure of macrophages to fine dust induced the productions of nitric oxide (NO), prostaglandin E 2 (PGE 2 ), and the mRNA expression levels of inflammatory mediators such as inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 whereas it was significantly attenuated by the treatment of dieckol. In addition, fine dust increased the pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α that were down-regulated by dieckol. Interestingly, dieckol protected macrophages against cell damages via reducing the fine dust-caused intracellular reactive oxygen species (ROS) generation via induction of superoxide dismutase production as well as the HO-1/Nrf2 signaling activation. In conclusion, dieckol protects RAW 264.7 cells against fine dust-induced inflammation and oxidative stress via inducing anti-inflammatory and antioxidant mechanisms.