Chromene suppresses activated inflammatory mediators in lipopolysaccharide-stimulated RAW 264.7 cells

Abstract

Inflammation is complex process in which a variety of immune cells are involved to defense from certain stimuli in the mammal’s body. However, it has been reported that over generated pro-inflammatory cytokines and mediators could get worse as disease or cancer. To find natural effective remedial agent for inflammation, in this study, we isolated functional algal compound from Sargassum siliquastrum, collected from Jeju Island of Korea, which were named as sargachromanol D (SD), a kind of chromene. And then we evaluated the anti-inflammatory effect of SD on lipopolysaccharide (LPS)-exposed RAW 264.7 cells through determining cell viability, cytotoxicity, production of inflammatory mediators (NO, PGE2, iNOS, COX-2), and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). As a result, SD inhibited production of nitric oxide (NO) and prostaglandin E2 (PGE2) on LPS-induced cells by preventing the expression of inflammatory mediators such as inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Concurrently, cytokines like TNF-α, IL-1β, and IL-6 causing inflammatory response were gradually restrained according to increasing concentration of SD. In addition, SD played a role in frustrating the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinases (MAPKs) pathways in a concentration-dependent manner. These findings sue as disease or cancer. To find natural effective remedial agent for inflammation, in this study, we isolated functional algal compound from Sargassum siliquastrum, collected from Jeju Island of Korea, which were named as sargachromanol D (SD), a kind of chromene. And then we evaluated the anti-inflammatory effect of SD on lipopolysaccharide (LPS)-exposed RAW 264.7 cells through determining cell viability, cytotoxicity, production of inflammatory mediators (NO, PGE2, iNOS, COX-2), and pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). As a result, SD inhibited production of nitric oxide (NO) and prostaglandin E2 (PGE2) on LPS-induced cells by preventing the expression of inflammatory mediators such as inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Concurrently, cytokines like TNF-α, IL-1β, and IL-6 causing inflammatory response were gradually restrained according to increasing concentration of SD. In addition, SD played a role in frustrating the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinases (MAPKs) pathways in a concentration-dependent manner.