甲基黄酮醇胺对血小板花生四烯酸代谢通路的影响

甲基黄酮醇胺(MPA)40mg·Kg~(-1)iv,能使花生四烯酸(AA)诱发的小鼠死亡率降低61％.MFA12.5～200μmol·L~(-1)呈剂量依赖性地抑制AA诱导的免血小板聚集.聚集率为49％±10％～4％±4%,对照组为69％±3％.MFA0.1～0.4mmol·L~(-1)呈剂量依赖性抑制AA诱导兔的血小板丙二醛(MDA)的生成,为(nmol·10~(-9)血小板)0.075±0.011～0.111±0.023,对照组为0.170±0.017.MFA0.4 mmol·L~(-1)有效地抑制凝血酶和A A诱导的兔血小板内MDA生成.分别为0.016±0.006.0.080±0.017,对照组分别为0.048±0006,0.160±0.025;普萘洛尔仅抑制凝血酶诱导的MDA生成.对AA诱导的MDA无影响.MFA0.4mmol·L~(-1)不影响血小板内cAMP含量.结果提示MFA抑制血小板AA代谢通路可能是其抑制血小板聚集功能的机理之一.

Effects of methylflavonolamine on arachidonic acid metabolism pathway of platelet

Effects of methylflavonolamine (MFA) on arachidonic acid(AA) metabolism pathway were studied. MFA (iv 40 mg · kg-1) lightened the acute pulmonary thromboenblism signs in mice and reduced the mortality induced by AA. MFA(12. 5~200μmol · L-1) in vitro dose-dependently inhibited rabbit platelet aggregation induced by AA. MFA(0.1~0. 4mmol · L-1) in vitro dose - dependently inhibited rabbit platelet malondiadehyde(MDA) formation in-duced by AA. MFA(0. 4mmol·L-1) inhibited platelet MDA formation in rabbits induced by thrombin and AA. While propranolol inhibited MDA formation induced by thrombin but not by AA. MFA (0.4 mmol · L-1) did not affect cAMP content in rabbit platelet. These results suggest that inhibitory effect of MFA on platelet AA metabolism may be one of the mechanism by which MFA inhibited platelet aggregation.