Proteomic analysis reveals the mechanisms of the astaxanthin suppressed foam cell formation

Abstract

AimsLipid metabolism in macrophages plays a key role in atherosclerosis development. Excessive low-density lipoprotein taken by macrophages leads to foam cell formation. In this study, we aimed to investigate the effect of astaxanthin on foam cells, and using mass spectrometry-based proteomic approaches to identified the protein expression changes of foam cells. Main methodsThe foam cell model was build, then treated with astaxanthin, and tested the content of TC and FC. And proteomics analysis was used in macrophage, macrophage-derived foam cells and macrophage-derived foam cells treated with AST. Then bioinformatic analyses were performed to annotate the functions and associated pathways of the differential proteins. Finally, western blot analysis further confirmed the differential expression of these proteins. Key findingsTotal cholesterol (TC) while free cholesterol (FC) increased in foam cells treated with astaxanthin. The proteomics data set presents a global view of the critical pathways involved in lipid metabolism included PI3K/CDC42 and PI3K/RAC1/TGF-β1 pathways. These pathways significantly increased cholesterol efflux from foam cells and further improved foam cell-induced inflammation.Significance: The present finding provide new insights into the mechanism of astaxanthin regulate lipid metabolism in macrophage foam cells.