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

Aims: Lipid 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 ef-fect of astaxanthin on foam cells, and using mass spectrometry-based proteomic approaches to identified the protein expression changes of foam cells.Main methods: The 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 findings: Total 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-beta 1 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 meta-bolism in macrophage foam cells.

Automated summary

This study aimed to investigate the effect of astaxanthin on foam cells and identified the protein expression changes using proteomic approaches. The results showed that total cholesterol and free cholesterol increased in foam cells treated with astaxanthin. Proteomics analysis revealed the involvement of PI3K/CDC42 and PI3K/RAC1/TGF-beta 1 pathways in lipid metabolism and cholesterol efflux, leading to reduced inflammation in foam cells. These findings provide new insights into the mechanism of astaxanthin in regulating lipid metabolism in macrophage foam cells.