Watson S P, Ruggiero M, Abrahams S L, Lapetina E G
J Biol Chem. 1986 Apr 25;261(12):5368-72.
Inositol 1,4,5-trisphosphate induces aggregation and the release of [3H]5-hydroxytryptamine from human platelets rendered permeable with saponin. This action of inositol 1,4,5-trisphosphate is associated with a significant formation of thromboxane B2, activation of phospholipase C, and phosphorylation of 20,000- and 40,000-dalton proteins, which are the substrates for myosin light chain kinase and protein kinase C, respectively. All of these responses are blocked by the cyclooxygenase inhibitors indomethacin and aspirin and the dual cyclooxygenase and lipoxygenase inhibitor 3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline (BW 755C). These data indicate that platelet activation by inositol 1,4,5-trisphosphate is initiated by the mobilization of Ca2+, which leads to phospholipase A2 activation. The thromboxanes and endoperoxides that are subsequently generated then induce activation via cell surface receptors.
肌醇1,4,5 -三磷酸可诱导经皂角苷处理而具有通透性的人血小板发生聚集并释放[3H]5 -羟色胺。肌醇1,4,5 -三磷酸的这一作用与血栓素B2的大量形成、磷脂酶C的激活以及20000道尔顿和40000道尔顿蛋白质的磷酸化有关，这两种蛋白质分别是肌球蛋白轻链激酶和蛋白激酶C的底物。所有这些反应均被环氧化酶抑制剂吲哚美辛和阿司匹林以及环氧化酶和脂氧合酶双重抑制剂3 -氨基-1 -[间-(三氟甲基)苯基]-2 -吡唑啉（BW 755C）所阻断。这些数据表明，肌醇1,4,5 -三磷酸对血小板的激活是由Ca2+的动员引发的，Ca2+的动员导致磷脂酶A2激活。随后生成的血栓素和内过氧化物再通过细胞表面受体诱导激活。
