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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.
Methyl flavonolamine (MPA) 40mg · Kg -1 iv reduced the mortality of arachidonic acid (AA) -induced mice by 61% .MFA12.5 ~ 200μmol·L -1 The dose-dependent inhibition of AA-induced platelet aggregation was 49% ± 10% ± 4% ± 4% in the control group and 69% ± 3% in the control group.MFA 0.1 ~ 0.4mmol·L ~ (-1) The dose-dependent inhibition of AA-induced platelets malondialdehyde (MDA) production was 0.075 ± 0.011 ~ 0.111 ± 0.023 (nmol · 10 -9 platelets) and 0.170 ± 0.017 in the control group L ~ (-1) effectively inhibited thrombin and AA-induced MDA production in rabbit platelets, respectively, which were 0.016 ± 0.006.0.080 ± 0.017 and 0.048 ± 0006 and 0.160 ± 0.025 respectively in the control group; propranolol only inhibited the clotting Enzyme-induced MDA production had no effect on AA-induced MDA.MFA 0.4 mmol·L -1 did not affect platelet cAMP content.The results suggest that MFA inhibits platelet AA metabolic pathway may be one of the mechanisms of its inhibition of platelet aggregation .