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Danshensu Promotes Cholesterol Efflux in RAW264.7 Macrophages

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Lipids

Abstract

Contemporary research suggests that macrophage foam cell and cholesterol efflux defect play pivotal role in atherogenesis. We reported on the heretofore unknown therapeutic effect of Danshensu (DSS) in reducing intracellular cholesterol level and unraveled the mechanism of DSS promotes cholesterol efflux. Oxidized low-density lipoprotein stimulation of Raw264.7 cells into foam cells, which were treated with DSS and co-treated with Simvastatin and Rosiglitazone. PPARγ, ABCA1, ABCG1, SR-BI, CD36, and LXR-α mRNA were quantified by Real-Time PCR. Western blotting was used to determine protein expression of PPARγ, ABCA1 and CD36. Cellular cholesterol handling was studied by measurement of intracellular lipid droplets concentration and cholesterol efflux. DSS significantly reduced scavenger receptor CD36 and its orthologue SR-BI. In addition, DSS stimulated the upregulation of cellular cholesterol exporters ABCA1 and ABCG1 to reduce intracellular lipid accumulation. DSS can reduce lipid deposition in Raw264.7 foam cells by balancing CD36 and ABCA1 protein expression.

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Abbreviations

ABCA1:

ATP-binding cassette transporter A1

ABCG1:

ATP-binding cassette transporter G1

CE:

Cholesteryl ester

FC:

Free cholesterol

HDL:

High-density lipoprotein

LXR-α:

Liver X receptor alpha

LDL:

Low-density lipoprotein

Ox-LDL:

Oxidized low-density lipoprotein

PPARγ:

Peroxisome proliferator-activated receptor gamma

RCT:

Reverse cholesterol transport

SR-BI:

Scavenger receptor class B type I

TC:

Total cholesterol

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Acknowledgments

This work was support by a grant from the National Key Basic Research Program of China (973 Program) (No. 2014CB542902), the National Natural Science Foundation of China (81273891), and the Program for Changjiang Scholars and Innovative Research Team in University (IRT1276).

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Correspondence to Guanwei Fan.

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Gao, H., Li, L., Li, L. et al. Danshensu Promotes Cholesterol Efflux in RAW264.7 Macrophages. Lipids 51, 1083–1092 (2016). https://doi.org/10.1007/s11745-016-4178-1

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  • DOI: https://doi.org/10.1007/s11745-016-4178-1

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