尖吻蝮蛇血凝酶止血作用的机制  

Hemostatic mechanism of agkistrodon heamocoagulase

作　　者：米鹏程[1] 黄莹[1] 孔焕育[1] 曹莹[1] 金宏[1] 庞建新[1] 

机构地区：[1]南方医科大学药学院,广州510515

出　　处：《中国新药杂志》2013年第11期1315-1319,1324,共6页Chinese Journal of New Drugs

基　　金：国家自然科学基金(81273577/H3109)

摘　　要：目的:考察注射用尖吻蝮蛇血凝酶(saculin)止血作用的机制。方法:通过分析saculin对纤维蛋白原、凝血因子XIII(FXIII)、凝血因子X(FX)和凝血酶原的直接作用探讨其止血机制及对血液系统的影响。结果:saculin能水解纤维蛋白原释放A肽(FpA)和少量的B肽(FpB),不激活FXIII、FX和凝血酶原,但其形成的纤维蛋白单体能利用FXIIIa和Ca2+通过共价交联形成多聚体。结论:saculin在出血局部通过水解纤维蛋白原释放出FpA和少量FpB,利用FXIIIa形成稳定的纤维蛋白凝块而止血;而在未损伤的血管内,sa-culin作为单一成分,不会引起血管内栓塞、弥散性血管内凝血等并发症。Objective： To investigate the hemostatic mechanism of agkistrodon heamocoagulase （saculin）. Methods： The effect of saculin on blood system and the hemostatic mechanism were investigated by analyzing the direct actions of saculin on fibrinogen, coagulation factor XIII, coagulation factor X and prothrombin. Results： Saculin was able to release fibrinopeptide A （FpA） and a small amount of fibrinopeptide B （FpB） from fibrinogen, but did not promote activation of the coagulation factor XIII, coagulation factor X and prothrombin. The fibrin monomers formed by saculin came together to form fibrin polymers by covalent cross-linking in the presence of coagulation factor XIIIa and Ca2＋. Conclusion： Saculin exerts its hemostatic effects in hemorrhagic area by hydrolyzing fibrinogen, releasing FpA and a small amount of FpB to generate insoluble fibrin clots by using coagulation factor XIIIa. However, saculin, as a single-ingredient, has no effect on intravascular embolization, disseminated intravascular coagulation and other complications in blood vessels.

关 键 词：尖吻蝮蛇血凝酶 止血机制 纤维蛋白原 凝血因子XIII 凝血因子X 凝血酶原 

分 类 号：R973[医药卫生—药品]