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首页> 外文期刊>Acta Pharmacologica Sinica >Calcium-dependent synergistic interaction of platelet activating factor and epinephrine in human platelet aggregation
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Calcium-dependent synergistic interaction of platelet activating factor and epinephrine in human platelet aggregation

机译：钙激活因子与肾上腺素在人血小板聚集中的钙依赖性协同相互作用

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AIM: To investigate the mechanism (s) involved in the synergistic interaction of platelet activating factor (PAF) and epinephrine. METHODS: Blood was obtained from healthy human subjects reported to be free of medications for at least two weeks before sampling. Aggregation was monitored at 37 ℃ using Dual-channel Lumi-aggregometer. The resulting aggregation was recorded for 5 min by the measurement of light transmission as a function of time. RESULTS: Platelet aggregation mediated by subthreshold concentrations of PAF (5-8 nmol/L) plus epinephrine (0.5-2 (μm ol/L) was inhibited by α_2-receptor blocker, yohimbine, and PAF receptor antagonist WEB 2086. This synergism was inhibited by calcium channel blockers, verapamil and diltiazem. In addition, platelet aggregation by co-addition of PAF and epinephrine was also inhibited by very low concentrations of phospholipase C (PLC) inhibitor (U73122; IC_(50)=0.2 μmol/L), the MAP kinase inhibitor, PD 98059 (IC_(50)=3 μmol/L), and cyclooxygenase (COX-1) inhibitors including indomethacin (IC_(50)=0.25 (μmol/L), flurbiprofen (IC_(50)=0.7 μmol/L), and piroxicam (IC_(50)=7 μmol/L). However, COX-2 inhibitors, nimesulide (IC_(50)=26 μmol/L), NS-398 (IC_(50)=7 μmol/L), and etodolac (1C_(50)=15 μmol/L) were also effective in inhibiting the aggregation. The inhibitors of protein kinase C (chelerythrine) and tyrosine kinase (genistien), and phosphatidylinositol 3-kinase inhibitor (wortmannin) had no significant effect on platelet aggregation induced by PAF and epinephrine. CONCLUSION: The synergistic effect of PAF and epinephrine on human platelet aggregation is receptor-mediated and involves the activation of PLC/Ca~(2+), COX and MAP kinase signalling pathways.
机译：目的：探讨血小板活化因子（PAF）与肾上腺素协同相互作用的机制。方法：从健康的人类受试者获得血液，据报道在采样前至少有两周没有药物治疗。使用双通道Lumi凝集计在37℃监测聚集。通过测量作为时间的函数的透光率，记录所得的聚集5分钟。结果：α_2受体阻滞剂，育亨宾和PAF受体拮抗剂WEB 2086抑制了亚阈浓度PAF（5-8 nmol / L）加肾上腺素（0.5-2（μmol / L）介导的血小板聚集。这种协同作用是钙离子通道阻滞剂，维拉帕米和地尔硫卓均具有抑制作用；此外，PAF和肾上腺素共添加引起的血小板聚集也受到极低浓度的磷脂酶C（PLC）抑制剂的抑制（U73122； IC_（50）= 0.2μmol/ L） ，MAP激酶抑制剂PD 98059（IC_（50）= 3μmol/ L）和环加氧酶（COX-1）抑制剂包括消炎痛（IC_（50）= 0.25（μmol/ L），氟比洛芬（IC_（50）= 0.7μmol/ L）和吡罗昔康（IC_（50）= 7μmol/ L）。但是，COX-2抑制剂尼美舒利（IC_（50）= 26μmol/ L），NS-398（IC_（50）= 7 （μmol/ L）和依托度酸（1C_（50）= 15μmol/ L）也有效抑制聚集；蛋白激酶C（白屈菜红碱）和酪氨酸激酶（genistien）抑制剂，以及磷脂酰肌醇3激酶抑制剂（渥曼青霉素） ） 哈d对PAF和肾上腺素诱导的血小板聚集没有明显影响。结论：PAF和肾上腺素对人血小板聚集的协同作用是受体介导的，涉及PLC / Ca〜（2 +），COX和MAP激酶信号通路的激活。

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