The effect of chrysanthemum morifolium Ramat extracts on ox-LDL-induced adhesion molecule ICAM-1 expression in Human umbilical vein endothelial cells

• Main Authors: Yun-Sheng, 解韻笙
• Other Authors: Chong-Kuei Lii
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/23714448233729001401

碩士 === 中山醫學大學 === 營養學研究所 === 95 === Oxidized low density lipoprotein (ox-LDL) has been known to be one of the atherogenic risk factors by numerous epidemiological, clinical, and animal studies. Ox-LDL induction of endothelial adhesion molecule expression is required for monocytes adhereing to endothelial cells. In this study, we intended to examine the effect of hot water extract (HYC) and 95% ethanol extract of yellow chrysanthemum morifolium Ramat (EYC) on ox-LDL-induced ICAM-1 expression in human umbilical vein endothelial cells (HUVECs). Result showed that HYC and EYC dose-dependently inhibit conjugated diene formation and TBARS in LDL induced by Cu2SO4 (p <0.05). Immunoblot assay showed that HYC (0.25-1 mg/ml) and EYC (25-250 μg/ml) inhibit intracellular ICAM-1 expression in a dose-dependent manner. An inhibition of 35.4% and 16.9% ICAM-1 expression was noted in cells treated with 1 mg/ml HYC and 250 μg/ml EYC, respectively .In addition of cellular ICAM-1, the cell surface expression of ICAM-1 was also inhibited by 22.4% and 14.7% in cells treated with 100 μg/ml HYC and 25 μg/ml EYC , respenctively. DCF-DA assay indicated HYC and EYC dose-dependently inhibit intracellular ROS production. The contents of phenolic compounds and flavonoids were 58.7 ± 3.4 mg gallic acid equivalents, 22.2 ± 1.1 mg quercetin equivalents/g dry HYC and were 44.5 ± 3.3 mg gallic acid equivalents and 19.3 ± 1.1 mg quercetin equivalents/g of dry EYC. Both phenolic compounds and flavoinids contents of HYC were higher than that of EYC. These findings suggest that both HYC and EYC effectively protect LDL against Cu2SO4 induced have antioxidant activity oxidation, and they are also protect in suppression of intracellular and cell surface ICAM-1 expression and intracellular ROS production in HUVECs.