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A more recent version of this article appeared on September 1, 2006

Papers In Press, published online ahead of print June 28, 2006
J. Lipid Res., doi:10.1194/jlr.M600226-JLR200
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Submitted on May 22, 2006
Revised on June 28, 2006
Accepted on June 28, 2006

NO-1886 suppressing atherosclerosis in high-fat/ high-sucrose/ high-cholesterol fed Bama minipigs is related to upregulating ATP-binding Cassette Transporter A1

Chi Zhang, Weidong Yin, Duanfang Liao, Liang Huang, Chaoke Tang, Kazuhiko Tsutsumi, Zongbao Wang, Yi Liu, Qinkai Li, Hongjie Hou, Manbo Cai, and Junxia Xiao

Institute of Cardiovascular Research, Nanhua University, Hengyang, Hunan 421001

Corresponding Author: wdy20012001{at}yahoo.com

ABSTRACT Objectives: It is widely believed that high-density lipoprotein cholesterol (HDL-C) functions to transport cholesterol from peripheral cells to the liver by reverse cholesterol transport (RCT), a pathway that may protect against atherosclerosis by clearing excess cholesterol from arterial cells. A cellular ATP-binding cassette transporter (ABC) called ABCA1 mediates the first step of RCT. NO-1886 has been proven to be highly effective in raising HDL-C and reducing atherosclerosis. However, the mechanism of inhibiting atherosclerosis for NO-1886 is not fully understood. Methods and results: In this study, the effects of NO-1886 on ABCA1 were investigated in high-fat/ high-sucrose/ high-cholesterol fed Chinese Bama minipigs. Administration of NO-1886 (0.1g/kg body weight/day) in the diet for five months significantly reduced atherosclerosis lesions, and significantly increased plasma HDL-C and apolipoprotein A-I levels. The mRNA and protein levels of ABCA1 in the liver, retroperitoneal adipose tissue and aorta were increased by NO-1886 as well. Multivariate linear regression analysis showed that the levels of lipoprotein lipase (LPL) in plasma and the levels of ABCA1 in aorta were independently associated with the atherosclerotic lesion area. In addition, NO-1886 up-regulated Liver X Receptor a (LXRa) and affected expression of scavenger receptor-type B class 1 (SR-BI) in the liver. Conclusion: These results demonstrated that the mechanism of inhibiting atherosclerosis for NO-1886 is associated with its effect on ABCA1.


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