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Korean red ginseng attenuates hypercholesterolemia‐enhanced platelet aggregation through suppression of diacylglycerol liberation in high‐cholesterol‐diet‐fed rabbits
Author(s) -
Hwang SeockYeon,
Son Dong Ju,
Kim IlWoong,
Kim DongMan,
Sohn SangHyun,
Lee JungJin,
Kim SiKwan
Publication year - 2008
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2363
Subject(s) - ginseng , liberation , platelet , arachidonic acid , cholesterol , diacylglycerol kinase , thrombus , chemistry , platelet activation , platelet aggregation , pharmacology , platelet adhesiveness , atheroma , thrombin , medicine , endocrinology , biochemistry , protein kinase c , in vitro , alternative medicine , pathology , enzyme
Intake of Korean red ginseng (KRG, ginseng Radix rubra), rich in glycosylated saponins (ginsenosides), has been known to inhibit platelet aggregation in the normocholesterolemic condition. However, it is unclear whether KRG can attenuate hypercholesterolemia‐enhanced platelet aggregation. This study examined whether the daily consumption of a KRG‐water extract (WE) could prevent the hypercholesterolemia‐enhanced platelet aggregation and progression of hypercholesterolemic atherosclerosis. KRG‐WE administration (200 mg/kg/day) for 8 weeks potently inhibited the platelet aggregation induced by low doses of agonists (0.5 µg/mL collagen and 0.025 unit/mL thrombin), whereas it weakly reduced the blood‐cholesterol levels and formation of atheromatous lesions. In further investigation, KRG‐WE significantly suppressed collagen‐induced 1,2‐diacylglycerol liberation, but had no significant effect on arachidonic acid liberation. Taken together, it can be suggested that the antiplatelet effect of KRG‐WE may, at least partly, be due to the inhibition of 1,2‐diacylglycerol generation rather than regulation of blood lipid levels. In conclusion, daily consumption of KRG‐WE could be a useful alternative measure for the prevention of thrombus and atheroma formation in hypercholesterolemia. Copyright © 2008 John Wiley & Sons, Ltd.

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