Abstract
The inflammatory reaction in large blood vessels involves up-regulation of vascular adhesion molecules such as endothelial cell selectin (E-selectin), soluble vascular cell adhesion molecule (sVCAM)-1, and soluble intercellular adhesion molecule (sICAM)-1. These vascular dysfunctions are associated with the development of atherosclerosis. β-Amyrin, an active component of Euphorbia hirta L., has potent anti-inflammatory effects. So far, its preventive effects against the expression of inflammatory mediator-induced adhesion molecules have not been investigated. Endothelial cells (SVEC4-10 cell line) were treated with 50% RAW conditioned media (i.e., normal SVEC4-10 culture media contains 50% of lipopolysaccharide-activated macrophage culture media) without or with β-amyrin (0.6 and 0.3 µM). The production levels of E-selectin, sICAM-1, and sVCAM-1 in the SVEC4-10 cells were measured with ELISA assay kits. Under the same treatment conditions, expression of endothelin (ET)-1 and endothelial type of NO synthase (eNOS) mRNA were analyzed by RT-PCR and agarose gel. With β-amyrin, the 50% RAW conditioned media-induced E-selectin, sICAM-1, and sVCAM-1 levels as well as ET-1 gene expression were all suppressed. β-Amyrin treatment also restored the 50% RAW conditioned media-suppressed eNOS mRNA expression. These data indicate that β-amyrin is potentially useful in preventing chronic inflammation-related vascular diseases.
Highlights
Inflammation is the pivotal pathologic mechanism of atherosclerosis and contributes to all of its stages, from plaque initiation to growth and rupture [1]
E-selectin production in SVEC4-10 endothelial cells was significantly induced by 50% RAW conditioned medium treatment (p < 0.005, Figure 2) compared to normal culture medium-treated endothelial cells
There was about 5-fold increase in soluble intercellular adhesion molecule (sICAM)-1 production when SVEC4-10 endothelial cells were cultured with the 50% RAW conditioned medium (p < 0.005, Figure 3)
Summary
Inflammation is the pivotal pathologic mechanism of atherosclerosis and contributes to all of its stages, from plaque initiation to growth and rupture [1]. Leukocyte recruitment is closely dependent on circulating adhesion molecules (CAMs), which are expressed by the vascular endothelium and believed to play a role in the initiation of the atherosclerotic process. E-selectin levels in the circulation have been applied to predict cardiovascular disease (CVD) risk in healthy women [4] and to reflect the severity of systemic atherosclerosis [5]. Elevated levels of soluble VCAM (sVCAM)-1 are associated with increased risk of coronary events in persons with existing CVD [11,12]. Since atherosclerosis has been recognized as a chronic inflammatory disease, here we investigated the possible preventive effects of β-amyrin on proinflammatory cytokines-mediated adhesion molecule production and expression of ET-1 and eNOS in endothelial cells
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