Published in:
01-04-2013
Phlorofucofuroeckol A Suppresses Expression of Inducible Nitric Oxide Synthase, Cyclooxygenase-2, and Pro-inflammatory Cytokines via Inhibition of Nuclear Factor-κB, c-Jun NH2-Terminal Kinases, and Akt in Microglial Cells
Authors:
A-Reum Kim, Min-Sup Lee, Ji-Woong Choi, Tadanobu Utsuki, Jae-Il Kim, Byeong-Churl Jang, Hyeung-Rak Kim
Published in:
Inflammation
|
Issue 2/2013
Login to get access
Abstract
Microglial activation has been implicated in many neurological disorders for its inflammatory and neurotrophic effects. In this study, we investigated the effects of phlorofucofuroeckol A isolated from Ecklonia stolonifera Okamura on the production of inflammatory mediators in lipopolysaccharide (LPS)-stimulated microglia. Pre-treatment of phlorofucofuroeckol A attenuated the productions of nitric oxide, prostaglandin E2, and pro-inflammatory cytokines in LPS-stimulated microglia. Profoundly, phlorofucofuroeckol A treatment showed inactivation of nuclear factor-κB (NF-κB) by preventing the degradation of inhibitor κB-α and the nuclear translocation of p65 NF-κB subunit. Moreover, phlorofucofuroeckol A inhibited the activation of c-Jun NH2-terminal kinases (JNKs), p38 mitogen-activated protein kinase (MAPK), and Akt, but not that of extracellular signal-regulated kinase. These results indicate that phlorofucofuroeckol A inhibits the LPS-induced expression of inflammatory mediators through inactivation of NF-κB, JNKs, p38 MAPK, and Akt pathways. These findings suggest that phlorofucofuroeckol A can be considered as a nutraceutical candidate for the treatment of neuroinflammation in neurodegenerative diseases.