Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages. (October 2015)

• Record Type: Journal Article
• Authors: Wang, Shuai; Zhang, Xue; Liu, Mingyue; Luan, Hong; Ji, Yubin; Guo, Peng; Wu, Chongming
• Is Part Of: Pharmaceutical biology. Volume 53:Number 10(2015:Oct.)
• Page Start: 1481
• Page End: 1487
• Publication Date: 2015-10
• Subjects: Pharmacognosy -- Periodicals; Materia medica, Vegetable -- Periodicals; 615.321
• DOI: 10.3109/13880209.2014.986688
• Languages: English
• ISSNs: 1388-0209

Abstract

<abstract> <title>Abstract</title> <p> <italic>Context</italic>: Chrysin, a natural flavonoid, has been shown to possess multiple pharmacological activities including anti-atherosclerosis.</p> <p> <italic>Objective</italic>: The effects of chrysin on foam cell formation and cholesterol flow in RAW264.7 macrophages were investigated in this work to explore the potential mechanism underlying its anti-atherogenic activity.</p> <p> <italic>Materials and methods</italic>: The inhibitive effect of chrysin on foam cell formation and cholesterol accumulation induced by oxidized low-density lipoprotein cholesterol (ox-LDL) was assessed by oil red O staining and intracellular total cholesterol and triglyceride quantification in RAW264.7 macrophages. The action of chrysin on cholesterol efflux and influx was tested by fluorescent assays. Real-time quantitative PCR was used to quantify the relative expression of cholesterol flow-associated genes and luciferase assay was applied to test the transcription activity of peroxisome proliferator-activated receptor gamma (PPARγ).</p> <p> <italic>Results</italic>: Chrysin dose dependently inhibited the formation of foam cells and prevented the enhanced cholesterol accumulation by ox-LDL. Treatment with chrysin (10 μM) significantly enhanced cholesterol efflux and substantially inhibited cholesterol influx. Simultaneously, chrysin significantly increased the mRNA levels of PPARγ, liver X receptor alpha (LXRα), ATP-binding cassette, sub-family A1 (ABCA1), and sub-family G1 (ABCG1), decreased scavenger receptor A1 (SR-A1) and SR-A2, and increased the transcriptional activity of PPARγ.</p> <p> <italic>Discussion and conclusion</italic>: Chrysin is a new inhibitor of foam cell formation that may stimulate cholesterol flow. Up-regulation of the classical PPARγ–LXRα–ABCA1/ABCG1 pathway and down-regulation of SR-A1 and SR-A2 may participate in its suppressive effect on intracellular cholesterol accumulation.</p> </abstract>