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目的研究补体调节蛋白ＣＤ５９通过阻止补体攻膜复合物（ＭＡＣ）的形成发挥其对依赖补体血小板损伤的保护作用。方法用连续柱层析从眼镜蛇粗毒中分离纯化出眼镜蛇毒因子（ＣＶＦ）。人红细胞膜经低渗破膜、超滤、木瓜蛋白酶消化、正丁醇抽提和连续柱层析分离纯化出补体调节蛋白ＣＤ５９。用ＣｈｒｏｎｏＬｏｇ型血小板聚集仪测定血小板变形、聚集和ＡＴＰ释放反应。结果预先加入ＣＤ５９可抑制ＣＶＦ引起的大白鼠血小板变形和ＡＴＰ释放，不影响ＣＶＦ引起的血小板聚集及粘附性增加。结论血小板膜表面形成的ＭＡＣ是补体激活引起血小板变形和ＡＴＰ释放的关键，ＣＤ５９对依赖补体血小板损伤有保护作用
Objective To investigate whether the complement regulatory protein CD59 exerts its protective effect on complement-dependent platelet damage by preventing the formation of complement-like membrane complex (MAC). Methods Cobra venom factor (CVF) was isolated and purified from cobra venom by continuous column chromatography. Human erythrocyte membrane was infiltrated by membrane, ultrafiltration, papain digestion, n-butanol extraction and continuous column chromatography to purify the complement regulatory protein CD59. Platelet deformability, aggregation and ATP release responses were measured using a Chrono-Log platelet aggregometer. Results Preadditive addition of CD59 inhibited CVF-induced platelet deformability and ATP release in rats and did not affect platelet aggregation and adherence induced by CVF. Conclusion The formation of MAC on the surface of platelet membrane is the key to complement activation induced platelet deformity and ATP release. CD59 has a protective effect on platelet-dependent platelet damage