Abstract
Sargassum serratifolium ethanolic extract has been known for strong antioxidant and anti-inflammatory properties. We prepared hexane fraction from the ethanolic extract of S. serratifolium (HSS) to improve biological activities. In this study, we investigated the effects of HSS on the inhibition of tumor necrosis factor (TNF)-α-induced monocyte adhesion to human umbilical vein endothelial cells (HUVECs). We found that HSS suppressed the production of cell adhesion molecules such as intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 in TNF-α-induced HUVECs. Moreover, TNF-α-induced production of monocyte chemoattractant protein 1 and keratinocyte chemoattractant was inhibited by HSS treatment. HSS suppressed TNF-α-induced nuclear factor kappa B (NF-κB) activation via preventing proteolytic degradation of inhibitor κB-α. HSS induced the production of heme oxygenase 1 via translocation of Nrf2 into the nucleus in TNF-α-treated HUVECs. Overall, HSS alleviated vascular inflammation through the downregulation of NF-κB activation and the upregulation of Nrf2 activation in TNF-α-induced HUVECs. These results indicate that HSS may be used as therapeutic agents for vascular inflammatory disorders.
Highlights
Vascular inflammation has been known to play a key role in the progress of atherosclerosis, and enhanced monocyte adhesion to endothelial cells is believed to be one of the earliest events in atherogenesis (Packard and Libby 2008)
Inhibitory effects (IC50) of these fractions on the adhesion molecules were determined with non-toxic concentration by Western blot using TNFα-stimulated human umbilical vein endothelial cells (HUVECs)
The quantification data suggest that the contents of sargahydroquinoic acid (SHQA), SCM, and sargaquinoic acid (SQA) in 100 g of meroterpenoid-rich extract from S. serratifolium (MES) were estimated to be 37.6 ± 2.1, 6.23 ± 0.36, and 1.89 ± 0.10 g, respectively (Kwon et al 2018)
Summary
Vascular inflammation has been known to play a key role in the progress of atherosclerosis, and enhanced monocyte adhesion to endothelial cells is believed to be one of the earliest events in atherogenesis (Packard and Libby 2008). Accumulating evidences have revealed that chronic inflammation plays a crucial role in the initiation and progression of atherosclerosis. Monocyte adhesion to endothelial cells is primarily mediated by several intracellular signaling events that lead to the elevated expression of endothelial adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) An accumulative evidence suggests that TNF-α, a pleiotropic pro-inflammatory cytokine in the inflammatory cascade, involves in a critical role in vascular inflammation and the subsequent progress of atherosclerosis. Approaches to regulate endothelial activation are potential strategies to prevent atherosclerosis through the suppression of vascular inflammation
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