Aqueous Extract of Tournefortia sarmentosa Stem Inhibits ADP-induced Platelet Aggregation

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Title:	Aqueous Extract of Tournefortia sarmentosa Stem Inhibits ADP-induced Platelet Aggregation
Authors:	Wang, LK (Wang, L. K.) Tsai, FM (Tsai, F. M.) Wu, S (Wu, S.) Lee, MC (Lee, M. C.) Tsai, TC (Tsai, T. C.) Chou, WM (Chou, Weimou) Wang, CH (Wang, C. H.)
Contributors:	生命科學系
Keywords:	P2Y(12) RECEPTOR SALVIANOLIC ACID CAFFEIC ACID WHOLE-BLOOD ACTIVATION MECHANISM THROMBOSIS ASPIRIN ANIMALS
Date:	2018
Issue Date:	2019-01-22 14:33:16 (UTC+8)
Abstract:	Tournefortia sarmentosa is a Chinese herbal medicine used as an antioxidant, detoxicant, and antiinflammatory agent. The present study evaluated the effect of T. sarmentosa on adenosine diphosphate-induced platelet aggregation. Our results showed that aqueous stem extract of T. sarmentosa inhibited adenosine diphosphate-induced platelet aggregation. In addition, we found components in T. sarmentosa, including caffeic acid, rosmarinic acid, salvianolic acid, play important roles in mediating adenosine diphosphate-induced platelet aggregation suppression. The stem extract of T. sarmentosa inhibited the adenosine diphosphate receptor P2Y(12)-mediated cyclic AMP production. Caffeic acid inhibited P2Y(1)-induced calcium influx. Furthermore, treatment of platelets with T. sarmentosa, or the components in stem extract of T. sarmentosa, suppressed adenosine diphosphate-induced release of thromboxane A2 and arachidonic acid and surface PAC-1 expression. These data demonstrate the aqueous stem extract of T. sarmentosa significantly suppressed platelet aggregation through P2Y(1) and P2Y(12) receptor signal pathways. The antiaggregation properties found in the stem extract of T. sarmentosa might help to prevent cardiovascular disease.
Appears in Collections:	[Department of Biology ] journal articles

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