RRC ID 58013
Author Manabe Y, Takii Y, Sugawara T.
Title Siphonaxanthin, a carotenoid from green algae, suppresses advanced glycation end product-induced inflammatory responses.
Journal J Nat Med
Abstract Advanced glycation end products (AGEs) induce inflammation and contribute to the pathogenesis of atherosclerosis. Although many studies have demonstrated the protective effects of carotenoids against atherosclerosis, the effects of carotenoids on AGE-induced inflammation have not been characterized. As such, we aimed to identify carotenoids that provided protection against AGE-elicited inflammation. AGE-stimulated RAW264 macrophages were first evaluated for NO generation. Among 17 carotenoids tested, only siphonaxanthin significantly suppressed it. Next, mRNA expression levels were measured in RAW264 macrophages and human umbilical vascular endothelial cells following siphonaxanthin and AGE treatment. Siphonaxanthin significantly suppressed AGE-induced mRNA expression of interleukin-6 and cellular adhesion molecules, which are known to be important for the pathogenesis of atherosclerosis. Siphonaxanthin also significantly suppressed endoplasmic reticulum (ER) stress marker genes. A reporter gene assay revealed that siphonaxanthin, as well as an ER stress inhibitor, significantly inhibited AGE-induced nuclear factor-κB (NF-κB) activation. Altogether, mitigation of ER stress and subsequent NF-κB activation is one of the molecular mechanisms by which siphonaxanthin suppressed AGE-elicited inflammation. Siphonaxanthin is a carotenoid commonly found in standard diets and is considered relatively safe for human consumption, and hence, dietary intake of siphonaxanthin or siphonaxanthin-containing green algae could be beneficial in lowering the risk of developing atherosclerosis.
Volume 74(1)
Pages 127-134
Published 2020-1-1
DOI 10.1007/s11418-019-01354-z
PII 10.1007/s11418-019-01354-z
PMID 31432315
MeSH Animals Cell Line Chlorophyta / chemistry* Endoplasmic Reticulum Stress / drug effects* Endothelial Cells / drug effects Enzyme Activation / drug effects Glycation End Products, Advanced / metabolism* Humans Inflammation / drug therapy* Interleukin-6 / immunology Mice NF-kappa B / metabolism RAW 264.7 Cells Xanthophylls / pharmacology*
IF 2.055
Times Cited 2
Human and Animal Cells RAW 264(RCB0535)