血小板激活因子（PAF-乙酰醚）的生物合成。II. 磷脂酶A2参与兔血小板中PAF-乙酰醚和溶血PAF-乙酰醚的形成。

Biosynthesis of platelet-activating factor (PAF-ACETHER). II. Involvement of phospholipase A2 in the formation of PAF-ACETHER and lyso-PAF-ACETHER from rabbit platelets.

作者信息

Benveniste J, Chignard M, Le Couedic J P, Vargaftig B B

出版信息

Thromb Res. 1982 Mar 1;25(5):375-85. doi: 10.1016/0049-3848(82)90128-1.

Abstract

The role of phospholipase A2 (PLA2) in the formation of platelet-activating factor (PAF-acether) by rabbit platelets is supported by several pieces of evidence. First, the release of PAF-acether was accompanied by that of its deacetylated analog, lyso-PAF-acether. Second, EDTA, EGTA, db-AMPc, p'-bromophenacylbromide and 874 CB, which, in spite of their structural diversity, are all PLA2 blockers, inhibited the release of both PAF-acether and of the lyso-compound. Third, addition of hog pancreas PLA2 to platelets as well as platelet lysis resulted in the release of lyso-PAF-acether, thus mimicking the metabolic events initiating formation of PAF-acether. These results indicate that PLA2 activation triggers both the second and the third pathway of platelet activation.

摘要

磷脂酶A2（PLA2）在兔血小板形成血小板活化因子（PAF - 乙酰醚）过程中的作用得到了多条证据的支持。首先，PAF - 乙酰醚的释放伴随着其脱乙酰化类似物溶血 - PAF - 乙酰醚的释放。其次，尽管EDTA、EGTA、二丁酰环磷腺苷（db - AMPc）、对溴苯甲酰溴和874 CB结构各异，但它们都是PLA2阻滞剂，可抑制PAF - 乙酰醚和溶血化合物的释放。第三，向血小板中添加猪胰PLA2以及血小板裂解都会导致溶血 - PAF - 乙酰醚的释放，从而模拟引发PAF - 乙酰醚形成的代谢事件。这些结果表明，PLA2激活触发了血小板活化的第二条和第三条途径。