花生四烯酰三氟甲基酮对胶原诱导的血小板活化的抑制作用。

Inhibition of collagen-induced platelet activation by arachidonyl trifluoromethyl ketone.

作者信息

McNicol A, Nickolaychuk B R

机构信息

Department of Oral Biology, University of Manitoba, Winnipeg, Canada.

出版信息

Biochem Pharmacol. 1995 Nov 27;50(11):1795-802. doi: 10.1016/0006-2952(95)02048-9.

DOI:10.1016/0006-2952(95)02048-9

PMID:8615857

Abstract

Collagen-induced platelet activation is associated with, and markedly potentiated by, the release of arachidonic acid and its subsequent conversion to thromboxane A2. The precise mechanism of arachidonic acid release is unknown. An inhibitor of isolated cytosolic phospholipase A2 (cPLA2), arachidonyl trifluoromethyl ketone (AACOCF3), was used to examine the role that cPLA2 plays in this process. AACOCF3 inhibited platelet aggregation in response to collagen and arachidonic acid but not to thrombin, calcium ionophore, phorbol ester, or a thromboxane mimetic. Thromboxane formation stimulated by thrombin or collagen was inhibited by AACOCF3. However, AACOCF3 did not inhibit collagen-induced [14C]arachidonic acid release. These data are consistent with the inhibitory effects of AACOCF3 on collagen-induced aggregation involving an action on the conversion of arachidonic acid to thromboxane.

摘要

胶原诱导的血小板活化与花生四烯酸的释放及其随后转化为血栓素A2相关，并被其显著增强。花生四烯酸释放的确切机制尚不清楚。使用一种分离的胞质磷脂酶A2（cPLA2）抑制剂——花生四烯酰三氟甲基酮（AACOCF3）来研究cPLA2在此过程中所起的作用。AACOCF3抑制血小板对胶原和花生四烯酸的聚集反应，但不抑制对凝血酶、钙离子载体、佛波酯或血栓素类似物的聚集反应。凝血酶或胶原刺激的血栓素形成受到AACOCF3的抑制。然而，AACOCF3并不抑制胶原诱导的[14C]花生四烯酸释放。这些数据与AACOCF3对胶原诱导的聚集的抑制作用一致，该抑制作用涉及对花生四烯酸转化为血栓素的作用。