Xu N, Zhou L, Ohlin A K, Nilsson A
Department of Medicine, University Hospital of Lund, Sweden.
Biochem Biophys Res Commun. 1995 Mar 17;208(2):765-72. doi: 10.1006/bbrc.1995.1403.
The effects of chylomicron-prothrombin complexes on platelet activation, including platelet aggregation, serotonin release, arachidonic acid release and increases of platelet cytosolic [Ca2+]i were examined. Furthermore the role of platelet factor Xa on the conversion of chylomicron bound prothrombin to thrombin was studied by using a synthetic inhibitor of factor Xa, TenStop. The chylomicron-prothrombin complexes could induce platelet aggregation and enhance the platelet serotonin release and arachidonic acid release in contrast to native chyle chylomicrons. An increase of platelet [Ca2+]i was observed during incubation with chylomicron-prothrombin complexes. TenStop inhibited platelet aggregation and serotonin release that were induced by chylomicron-prothrombin complexes in a dose-dependent manner, whereas the TenStop itself did not inhibit the platelet aggregation induced by thrombin and collagen. It is concluded that platelet activation induced by chylomicron-prothrombin complexes is related to the platelet factor Xa that could be the key factor in the conversion of chylomicron bound prothrombin to thrombin.
研究了乳糜微粒 - 凝血酶原复合物对血小板活化的影响,包括血小板聚集、5-羟色胺释放、花生四烯酸释放以及血小板胞质内[Ca2+]i升高。此外,通过使用Xa因子的合成抑制剂TenStop,研究了血小板Xa因子在乳糜微粒结合的凝血酶原转化为凝血酶过程中的作用。与天然乳糜微粒相比,乳糜微粒 - 凝血酶原复合物可诱导血小板聚集,并增强血小板5-羟色胺释放和花生四烯酸释放。在与乳糜微粒 - 凝血酶原复合物孵育期间,观察到血小板[Ca2+]i升高。TenStop以剂量依赖方式抑制乳糜微粒 - 凝血酶原复合物诱导的血小板聚集和5-羟色胺释放,而TenStop本身并不抑制凝血酶和胶原诱导的血小板聚集。得出的结论是,乳糜微粒 - 凝血酶原复合物诱导的血小板活化与血小板Xa因子有关,Xa因子可能是乳糜微粒结合的凝血酶原转化为凝血酶的关键因素。