Abstract
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 E2 (PGE2), 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.
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