Anti-atherosclerotic function of Astragali Radix extract: downregulation of adhesion molecules in vitro and in vivo

BMC Complementary and Alternative Medicine

Research Article

Jia-tao Feng¹  Xiu-li Zhang¹  Cheng-hui Yan²  Xiao-lin Zhang²  Yan Duan²  Shao-wei Liu²  Ya-ling Han³  Yang You⁴ 

[1] Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China;Department of Cardiology, Cardiovascular Research Institute, Shenyang Northern Hospital, Shenyang, China;Department of Cardiology, Cardiovascular Research Institute, Shenyang Northern Hospital, Shenyang, China;Department of Cardiology, Shenyang General Hospital, 83 Wenhua Road, 110840, Shenyang, China;Department of Cardiology, Cardiovascular Research Institute, Shenyang Northern Hospital, Shenyang, China;The Affiliated Hospital of Liaoning University of TCM, Shenyang, China;

关键词: Astragali Radix extract;    Vascular cell adhesion molecule-1;    Vntercellular adhesion molecule-1;    Apolipoprotein E-deficient mice;    Atherosclerosis;   

DOI  :  10.1186/1472-6882-12-54

 received in 2011-12-20, accepted in 2012-04-26,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundAtherosclerosis is considered to be a chronic inflammatory disease. Astragali Radix extract (ARE) is one of the major active ingredients extracted from the root of Astragalus membranaceus Bge. Although ARE has an anti-inflammatory function, its anti-atherosclerotic effects and mechanisms have not yet been elucidated.MethodsMurine endothelial SVEC4-10 cells were pretreated with different doses of ARE at different times prior to induction with tumor necrosis factor (TNF)-α. Cell adhesion assays were performed using THP-1 cells and assessed by enzyme-linked immunosorbent assay, western blotting and immunofluorescence analyses to detect the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), phosphorylated inhibitor of κB (p-iκB) and nuclear factor (NF)-κB. We also examined the effect of ARE on atherosclerosis in the aortic endothelium of apolipoprotein E-deficient (apoE−/−) mice.ResultsTNF-α strongly increased the expression of VCAM-1 and ICAM-1 accompanied by increased expression of p-iκB and NF-κB proteins. However, the expression levels of VCAM-1 and ICAM-1 were reduced by ARE in dose- and time-dependent manners, with the strongest effect at a dose of 120 μg/ml incubated for 4 h. This was accompanied by significantly decreased expression of p-iκB and inhibited activation of NF-κB. Immunofluorescence analysis also revealed that oral administration of ARE resulted in downregulation of adhesion molecules and decreased expression of macrophages in the aortic endothelium of apoE−/− mice. ARE could suppress the inflammatory reaction and inhibit the progression of atherosclerotic lesions in apoE−/− mice.ConclusionThis study demonstrated that ARE might be an effective anti-inflammatory agent for the treatment of atherosclerosis, possibly acting via the decreased expression of adhesion molecules.

【 授权许可】

Unknown   
© You et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.