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目的：研究蛋白酪氨酸磷酸化（ＰＴＰ）在血小板激活因子（ＰＡＦ）诱导血小板信号传导中的作用．方法：用水洗兔血小板考查Ｇｅｎ抑制聚集及５羟色胺释放，Ｆｕｒａ２和ＢＣＥＣＦ负载测胞内钙及ｐＨ，特异性抗酪氨酸单抗及免疫印迹法检测ＰＴＰ．结果：Ｇｅｎ１００和２００μｍｏｌ·Ｌ－１分别抑制ＰＡＦ诱导的５羟色胺释放为２３７％±２０％及４１％±８％，对胞内钙增加和Ｎａ＋／Ｈ＋交换也有抑制作用．ＰＡＦ增加Ｍｒ为７００００，６００００，５００００，４２０００／４００００，３４０００的ＰＴＰ．Ｇｅｎ２００，４００μｍｏｌ·Ｌ－１明显抑制该效应．用Ｓｔａ２０ｎｍｏｌ·Ｌ－１，ＢＡＰＴＡ２００μｍｏｌ·Ｌ－１，依他酸２ｍｍｏｌ·Ｌ－１，分别阻断ＰＫＣ及胞内钙增加和内流，也减少ＰＴＰ形成．结论：ＰＴＰ参与ＰＡＦ诱导血小板信号传导途径，ＰＫＣ活化和胞内钙动员对ＰＴＰ有调节作用．
AIM: To investigate the role of protein tyrosine phosphorylation (PTP) in platelet-activating factor (PAF) -induced platelet signaling. Methods: Rabbit platelets were washed with water to inhibit the aggregation and serotonin release of Gen, the intracellular calcium and pH of Fura2 and BCECF were tested, and the specific anti-tyrosine mAb and Western blot were used to detect PTP. Results: Gen100 and 200 μmol·L-1 inhibited the release of serotonin 5-hydroxytryptamine by 23.7% ± 2.0% and 41% ± 8%, respectively, and inhibited the increase of intracellular calcium and Na + / H + exchange. PAF increase Mr 70000, 60000, 50000, 4000/40000, 34000 PTP. Gen200,400μmol·L-1 significantly inhibited this effect. With Sta20nmol·L-1, BAPTA200μmol·L-1, Eta-acid 2mmol·L-1, respectively, blocking PKC and intracellular calcium increase and influx, but also reduce the formation of PTP. CONCLUSION: PTP is involved in PAF-induced platelet signal transduction pathway. PKC activation and intracellular calcium mobilization may regulate PTP.