Reduction of Adhesion Molecule Production and Alteration of eNOS and Endothelin-1 mRNA Expression in Endothelium by Euphorbia hirta L. through Its Beneficial beta-Amyrin Molecule

doi:10.3390/molecules190710534

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標題:	Reduction of Adhesion Molecule Production and Alteration of eNOS and Endothelin-1 mRNA Expression in Endothelium by Euphorbia hirta L. through Its Beneficial beta-Amyrin Molecule
作者:	Shih, Mei Fen Cherng, Jong Yuh
貢獻者:	藥學系
關鍵字:	E-selectin sICAM-1 sVCAM-1 Endothelin-1 mRNA eNOS mRNA beta-amyrin
日期:	2014-07
上傳時間:	2015-05-06 21:24:25 (UTC+8)
出版者:	Mdpi Ag
摘要:	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. beta-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 beta-amyrin (0.6 and 0.3 mu M). 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 beta-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. beta-Amyrin treatment also restored the 50% RAW conditioned media-suppressed eNOS mRNA expression. These data indicate that. beta-amyrin is potentially useful in preventing chronic inflammation-related vascular diseases.
關聯:	Molecules, v.19 n.7, pp.10534-10545
显示于类别:	[藥學系(所)] 期刊論文

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