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Emodin enhances cholesterol efflux through activation of peroxisome proliferator‐activated receptor‐gamma in oxidized low density lipoprotein‐loaded THP‐1 macrophages

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Clinical and Experimental Pharmacology and Physiology

Published online on


Peroxisome proliferator‐activated receptors‐gamma (PPAR‐γ) is a nuclear receptor involved in the regulation of lipid metabolism. In the present study, we sought to investigate the effects of emodin, an anthraquinone derivative isolated from the roots of Rheum palmatum, on PPAR‐γ signaling and cholesterol efflux in macrophage foam cells. Oxidized low density lipoprotein (oxLDL)‐stimulated THP‐1 macrophages were incubated with different concentrations of emodin (0‐10 μM) for 18 h. Western blot analysis and semi‐reverse transcription polymerase chain reaction were used to assess the expression of key genes involved in cholesterol efflux including PPAR‐γ, liver X receptor alpha (LXR‐α), ATP‐binding cassette transporter A1 (ABCA1), and ABCG1. The levels of apolipoprotein A‐I (apoA‐I)‐mediated cholesterol efflux in emodin‐treated cells were measured. PPAR‐γ mRNA and protein levels were increased in emodin‐treated cells in a time and dose‐dependent manner. Emodin treatment also resulted in a concentration‐dependent induction of LXR‐α, ABCA1, and ABCG1 expression. Moreover, emodin promoted apoA‐I‐mediated cholesterol efflux from oxLDL‐loaded THP‐1 macrophages, which were significantly abolished by pretreatment with the PPAR‐γ selective antagonist GW9662 or specific small interfering RNA for PPAR‐γ. Taken together, our results demonstrate that emodin promotes cholesterol efflux from THP‐1 macrophages through activation of the PPAR‐γ signaling pathway and may represent a potential anti‐atherosclerotic drug. This article is protected by copyright. All rights reserved.