蓝萼甲素对兔血小板生成血小板活化因子及花生四烯酸代谢的影响

Effects of glaucocalyxin A on PAF biosynthesis and arachidonic acid metabolism in washed rabbit platelets

蓝萼甲素在浓度0.1～100μmol·L^(-1)时可抑制A23187刺激的免血小板生成血小板活化因子,其IC_(50)为0.47μmol·L^(-1),当其浓度为10,100μmol·L^(-1)时能抑制花生四烯酸诱导的兔血小板血栓素A_2生成同时升高前列腺素E_2,推测蓝萼甲素通过抑制血小板活化因子生物合成及选择性抑制血栓素A_2生成而抑制血小板激活。

Washed rabbit platelets were incubated with A 23187 or arachidonic acid (AA) after being exposed to glaucocalyxin A, aspirin (Asp) or control solvent.Biosynthesized PAF was measured by the rabbit platelets aggregation and radioimmunoassay was used to investigate PGE2 and TXA2 production in rabbit platelets.Glaucocalyxin A could significantly inhibit the PAF biosynthesis in the range of 0.1 to 100 μmol·L-1. Meanwhile, it could decrease TXA2 level and increase PGE2 production at the concentration of more than 10μmol·L-1.It seemed that glaucocalyxin A inhibited the platelet activation through two pathways. (1) It inhibited PAF biosynthesis in low concentrations in rabbit platelets. (2) It blocked the pathway of thromboxane synthetase and changed the direction of arachidonic acid metabolism in platelets.Our results suggest that glaucocalyxin A is a new platelet inhibitor.