Add time:07/22/2019 Source:sciencedirect.com
ganodermic acid S (cas 112430-63-4) (GAS), isolated from the Chinese medicinal fungus Ganoderma lucidum (Fr.) Karst (Polyporaceae), exhibits inhibitory effects on platelet responses to various aggregating agonists. Our study demonstrated that GAS also participated in potentiating the response of human gel-filtered platelets to prostaglandin (PG) E1. GAS at <20 μM did not show any significant change of basal cyclic AMP level in gel-filtered platelets. However, GAS potentiated the PGE1-evoked cyclic AMP level in a bell-shaped, concentration-dependent manner. The agent at 7.5 μM enhanced the level up to 1.8-fold of that evoked by PGE1 alone. Collagen did not inhibit the PGE1-induced cyclic AMP level in platelets pretreated with GAS at 6 to 7.5 μM. In the presence of 7.5 μM GAS, the agent enhanced the inhibition of PGE1 on platelet response to collagen in: phosphorylation of myosin light chain and pleckstrin; α-granule secretion; cell aggregation and protein-tyrosine phosphorylation. In addition, the agent along with PGE1 almost abolished the dense-granule secretion and thromboxane (TX) B2 formation. The results suggest that GAS played an additional role in potentiating the PGE1-induced cyclic AMP synthesis. GAS and PGE1 inhibited additively the platelet response to collagen.
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