Castro-Faria-Neto H C, Martins M A, Silva P M, Bozza P T, Cruz H N, de Queiroz-Paulo M, Kaplan M A, Cordeiro R S
Departamento de Fisiologia e Farmacodinâmica, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.
J Lipid Mediat. 1993 May;7(1):1-9.
The ability of a furofuran lignan, epiyangambin, to inhibit PAF-induced rabbit platelet aggregation in vitro and thrombocytopenia in rats was investigated. Epiyangambin dose-dependently inhibited PAF-induced platelet aggregation without modifying the amplitude of the maximal response, indicating a competitive antagonism. The IC50 value of epiyangambin for 10(-9) M PAF-induced aggregation was 6.1 x 10(-7) M and the Schild analysis provided a pA2 of 6.91 +/- 0.2 with a slope of 0.98 +/- 0.25 (n = 4) and a pKb of 6.94 +/- 0.19. Epiyangambin had no effect upon the platelet aggregation induced by collagen, thrombin or ADP. The in vivo administration of the lignan at 20 mg/kg significantly inhibited PAF-induced thrombocytopenia in rats. These data indicate that epiyangambin is a potent and selective antagonist of PAF both in vitro and in vivo.
研究了呋喃呋喃木脂素表杨刚宾在体外抑制血小板活化因子（PAF）诱导的兔血小板聚集以及在体内抑制大鼠血小板减少的能力。表杨刚宾剂量依赖性地抑制PAF诱导的血小板聚集，且不改变最大反应幅度，表明其具有竞争性拮抗作用。表杨刚宾对10(-9) M PAF诱导的聚集的IC50值为6.1×10(-7) M，Schild分析得出pA2为6.91±0.2，斜率为0.98±0.25（n = 4），pKb为6.94±0.19。表杨刚宾对胶原、凝血酶或ADP诱导的血小板聚集没有影响。以20 mg/kg的剂量在体内给予该木脂素可显著抑制PAF诱导的大鼠血小板减少。这些数据表明，表杨刚宾在体外和体内都是一种有效的PAF选择性拮抗剂。
