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이동하,박화진,권혁우,김현홍,임덕휘,남기석,신정해,김종래,이종진,권호균 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.1
In this study, we investigated the effect ofcordycepin-enriched (CE)-WIB801C from Cordyceps militarison ADP (20 lM)-stimulated platelet aggregation. CE-WIB801C dose-dependently inhibited ADP-inducedplatelet aggregation, and its IC50 value was 18.5 lg/mL. CE-WIB801C decreased TXA2 production, but did notinhibit the activities of COX-1 and thromboxane synthase(TXAS) in ADP-activated platelets, which suggests that theinhibition of TXA2 production by CE-WIB801C is notresulted from the direct inhibition of COX-1 and TXAS. CE-WIB801C inhibited ATP release and [Ca2+]i mobilization,and increased cAMP level and IP3RI (Ser1756)phosphorylation in ADP-activated platelets. cAMP-dependentprotein kinase (A-kinase) inhibitor Rp-8-Br-cAMPSincreased CE-WIB801C-inhibited [Ca2+]i mobilization,and strongly inhibited CE-WIB801C-increased IP3RI(Ser1756) phosphorylation. CE-WIB801C elevated thephosphorylation of VASP (Ser157), an A-kinase substrate,but inhibited fibrinogen binding to aIIb/b3. These resultssuggest that CE-WIB801C-elevated cAMP involved inIP3RI (Ser1756) phosphorylation to inhibit [Ca2+]i mobilizationand, VASP (Ser157) phosphorylation to inhibit aIIb/b3 activation. Therefore, in this study, we demonstrate thatCE-WIB801C may have a preventive or therapeuticpotential for platelet aggregation-mediated diseases, suchas thrombosis, myocardial infarction, atherosclerosis, andischemic cerebrovascular disease.