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Open Access Research

The combination of L-4F and simvastatin stimulate cholesterol efflux and related proteins expressions to reduce atherosclerotic lesions in apoE knockout mice

Ru Ying1, Yong Yuan1*, Ya-Fei Qin1, Di Tian2, Li Feng1, Zhi-Gang Guo2, Yan-Xiang Sun1 and Ming-Xing Li1

Author Affiliations

1 Department of Cardiology, Zhongshan hospital, Sun Yat- Sen University, Zhongshan, Guang Dong, China

2 Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China

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Lipids in Health and Disease 2013, 12:180  doi:10.1186/1476-511X-12-180

Published: 8 December 2013



Both L-4F, one apolipoprotein A-1 mimetic peptide, and statins can reduce progression of atherosclerosis by different mechanisms. The combination of the two drugs can cause lesion regression by rendering HDL anti-inflammatory. We postulated that combination of L-4F and simvastatin may stimulate cholesterol efflux and related proteins expressions to alleviate atherosclerosis.


Thirty male wild-type (W-T) C57 BL/6 mice and apo E−/− mice were divided into five groups: W-T group, atherosclerosis (AS) group, simvastatin group, L-4F group and the combination of simvastatin and L-4F group. After 16 weeks, serum lipids, atherosclerotic lesion areas, cholesterol efflux and the expressions of related proteins including ABCA1, SR-BI, ABCG1, LXRα and PPARγ were evaluated.


The aortic atherosclerotic lesion areas were reduced more significantly by combination of both drugs than single agent, and cholesterol efflux was promoted more in combination group than simvastatin and L-4F group. Besides, the combination group promoted expressions of cholesterol efflux related proteins.


The combination of L-4F and simvastatin reduced atherosclerotic lesions, which stimulates cholesterol efflux by promoting the expressions of related proteins. In addition, these results help us further understand that the regression of the atherosclerosis would be assessed by reduction in LDL-C with increase of cholesterol efflux.

Atherosclerosis; High density Lipoprotein; Coronary artery disease; Apolipoprotein A-1 mimetic peptide; Statins