Abstract
The non-saponin fraction (NSF; lipophilic fraction) from the roots of Panax ginseng inhibited the aggregation of human platelets induced by thrombin (0.1 units/ml) in a dose-dependent manner. NSF induced the elevation of cGMP concentration in human platelets in a similar manner to molsidomine, a known vasodilator. NSF also inhibited Ca(2+)-influx into platelets. While verapamil, a Ca(2+)-antagonist, increased the cAMP level in platelets stimulated by thrombin, NSF had little effect on cAMP formation. Instead, NSF potently inhibited the thromboxane A2 (TXA2) production. The results suggest that NSF may regulate the levels of cGMP and TXA2 to inhibit platelet aggregation induced by thrombin.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Alkynes
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Blood Platelets / drug effects
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Calcium / metabolism
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Calcium Channel Blockers / pharmacology
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Cyclic AMP / biosynthesis
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Cyclic GMP / biosynthesis*
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Diynes
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Fatty Alcohols / pharmacology*
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Humans
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Molsidomine / pharmacology
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Panax*
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Plant Extracts / pharmacology
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Plants, Medicinal*
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Platelet Aggregation Inhibitors / pharmacology*
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Thrombin
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Thromboxane A2 / biosynthesis*
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Vasodilator Agents / pharmacology
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Verapamil / pharmacology
Substances
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Alkynes
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Calcium Channel Blockers
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Diynes
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Fatty Alcohols
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Plant Extracts
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Platelet Aggregation Inhibitors
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Vasodilator Agents
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falcarinol
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Thromboxane A2
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Verapamil
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Molsidomine
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Cyclic AMP
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Thrombin
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Cyclic GMP
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Calcium