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Pharm Biol. 2015;53(10):1481-7. doi: 10.3109/13880209.2014.986688. Epub 2015 Apr 10.

Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages.

Author information

1
Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences & Peking Union Medical College , Beijing , PR China and.

Abstract

CONTEXT:

Chrysin, a natural flavonoid, has been shown to possess multiple pharmacological activities including anti-atherosclerosis.

OBJECTIVE:

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.

MATERIALS AND METHODS:

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).

RESULTS:

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.

DISCUSSION AND CONCLUSION:

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.

KEYWORDS:

Atherosclerosis; PPARγ; cholesterol influx

PMID:
25857322
DOI:
10.3109/13880209.2014.986688
[Indexed for MEDLINE]

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