Danshensu Promotes Cholesterol Efflux in RAW264.7 Macrophages

被引：34

作者：

Gao, Hui ^{[1
,2
]}

Li, Lingyan ^{[1
,2
]}

Li, Lan ^{[1
,2
]}

Gong, Bo ^{[1
,2
]}

Dong, Pengzhi ^{[1
,2
]}

Fordjour, Patrick Asare ^{[1
,2
]}

Zhu, Yan ^{[1
,2
]}

Fan, Guanwei ^{[1
,2
]}

机构：

[1] Tianjin Univ Tradit Chinese Med, State Key Lab Modern Chinese Med, Tianjin 300193, Peoples R China

[2] Tianjin Univ Tradit Chinese Med, Minist Educ, Key Lab Pharmacol Tradit Chinese Med Formulae, 312 Anshanxi Rd, Tianjin 300193, Peoples R China

来源：

LIPIDS | 2016年 / 51卷 / 09期

基金：

中国国家自然科学基金;

关键词：

Danshensu (DSS); Atherosclerosis; Foam cell; Cholesterol efflux; SCAVENGER RECEPTOR; SR-BI; LIPID-ACCUMULATION; SELECTIVE UPTAKE; LIPOPROTEIN; CD36; HDL; ABCA1; METABOLISM; MECHANISMS;

D O I：

10.1007/s11745-016-4178-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. PPAR gamma, ABCA1, ABCG1, SR-BI, CD36, and LXR-alpha mRNA were quantified by Real-Time PCR. Western blotting was used to determine protein expression of PPAR gamma, 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.

引用

页码：1083 / 1092

页数：10

共 28 条

[1] CD36 inhibition prevents lipid accumulation and contractile dysfunction in rat cardiomyocytes [J].