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目的 研究两种 Ｃ Ｄ９ 单克隆抗体（ Ｍｃ Ａｂ） Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 对人血小板膜纤维蛋白原受体功能的调控作用及其可能的作用机制。方法 利用１２５ Ｉ标记人纤维蛋白原（ Ｆｇ） ，观察 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４作用下血小板 Ｆｇ 特异性结合量，反映血小板膜上 Ｆｇ 受体的暴露情况，并观察无 Ｆｇ 存在条件下，由 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 诱导的 Ｆｇ 受体暴露后的变化。结果 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 均能显著诱导血小板与 Ｆｇ 特异性结合，而在无 Ｆｇ 存在时，两种 Ｍｃ Ａｂ 诱导的 Ｆｇ 受体会很快“关闭”，失去结合 Ｆｇ 的能力；抑制蛋白激酶 Ｃ（ Ｐ Ｋ Ｃ） 活性，应用 Ａｓｐｉｒｉｎ 、 Ａｐｙｒａｓｅ 和（ 或） Ｐ Ｇ Ｉ２ 预处理血小板，能不同程度地抑制 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 诱导的血小板膜 Ｆｇ 受体暴露。结论 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 均能诱发血小板膜 Ｆｇ 受体暴露，两者诱发人血小板 Ｆｇ 受体暴露可能是三条途径综合作用的结果：即二磷酸腺苷释放、血栓烷生成和环磷酸腺苷途径，而 Ｐ Ｋ Ｃ激活可能是三条途径的共同通路。
Objective To investigate the regulation of human platelet membrane fibrinogen receptor function and its possible mechanism by two monoclonal antibodies (McAb) H I117 and S J9 A4. Methods 125I-labeled human fibrinogen (Fg) was used to observe the amount of Fg-specific binding of platelets to H117 and SJ9 A4 and to reflect the exposure of Fg receptors on platelets. In the absence of Fg, I117 and S J9 A4-induced Fg receptor changes after exposure. Results Both H117 and S J9 A4 significantly induced platelet binding to Fg, whereas in the absence of Fg, both Mc Ab-induced Fg receptors quickly “turned off”, losing the ability to bind to Fg; inhibiting protein kinase C (P K C) activity. Pretreatment of platelets with Aspirin, Apyrase and / or P G 12 inhibited the exposure of platelet Fg receptors induced by H I117 and S J9 A4 to varying degrees. Conclusions H I117 and S J9 A4 all induce platelet Fg receptor exposure. The exposure of platelet Fg receptors induced by both may be the result of three pathways: release of adenosine diphosphate, formation of thromboxane and cyclic adenosine monophosphate Pathway, and P K C activation may be the common pathway of the three pathways.