Abstract
The root of Cynanchum wilfordii (C. wilfordii) contains several biologically active compounds which have been used as traditional medicines in Asia. In the present study, we evaluated the anti-inflammatory effects of an ethanol root extract of C. wilfordii (CWE) on tumor necrosis factor (TNF)-α-stimulated human aortic smooth muscle cells (HASMCs). The inhibitory effects of CWE on vascular cell adhesion molecule (VCAM)-1 expression under an optimum extraction condition were examined. CWE suppressed the expression of VCAM-1 and ICAM-1 and the adhesion of THP-1 monocytes to the TNF-α-stimulated HASMCs. Consistent with the in vitro observations, CWE inhibited the aortic expression of ICAM-1 and VCAM-1 in atherogenic diet-fed mice. CWE also downregulated the expression of nuclear factor-κB (NF-κB p65) and its uclear translocation in the stimulated HASMCs. In order to identify the active components in CWE, we re-extracted CWE using several solvents, and found that the ethyl acetate fraction was the most effective in suppressing the expression of VCAM-1 and ICAM-1. Four major acetophenones were purified from the ethyl acetate fraction, and two components, p-hydroxyacetophenone and cynandione A, potently inhibited the expression of ICAM-1 and VCAM-1 in the stimulated HASMCs. We assessed and determined the amounts of these two active components from CWE, and our results suggested that the root of C. wilfordii and its two bioactive acetophenones may be used for the prevention and treatment of atherosclerosis and vascular inflammatory diseases.
Highlights
We investigated the effects of the ethanol concentration for the root extract of C. wilfordii on the inhibition of the expression of adhesion molecules in the tumor necrosis factor-α (TNF-α)-stimulated human aortic smooth muscle cells (HASMCs)
We found that the ethanol extracts obtained with various concentrations had suppressive effects on tumor necrosis factor (TNF)-α-induced vascular cell adhesion molecule-1 (VCAM-1) expression in the HASMCs (Fig. 1)
Different values are represented by symbols (**P
Summary
Vascular inflammation is a complex and multifactorial pathophysiological process that plays a key role in the development and progression of various cardiovascular diseases, including atherosclerosis and congestive heart failure [1,2]. There are various risk factors involved, such as oxidative stress and modified low-density lipoprotein (LDL) cholesterol that may contribute to the onset and progression of vascular inflammation and result in chronic inflammation [3]. This process is predominantly mediated by a diverse group of cell adhesion molecules (CAMs), which are expressed on the surface of vascular endothelial cells and smooth muscle cells in response to several inflammatory stimuli [4]. The functional inhibition of CAMs may be a critical therapeutic strategy for the treatment of vascular diseases
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