Rho M C, Nakahata N, Ohizumi Y
Department of Pharmaceutical Molecular Biology, Faculty of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Jpn J Pharmacol. 1998 Jan;76(1):117-20. doi: 10.1254/jjp.76.117.
The marine toxin zooxanthellatoxin-A (ZT-A) and the Ca2+ ionophore ionomycin caused aggregation in rabbit platelets. While ZT-A-induced platelet aggregation was inhibited by indomethacin, ionomycin-induced aggregation was potentiated by the drug. In contrast, both ZT-A- and ionomycin-induced accumulations of thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2), were completely inhibited by indomethacin. 12S-Hydroxyeicosatetraenoic acid (12-HETE), which could be accumulated in the presence of indomethacin, inhibited ZT-A-induced aggregation, but it potentiated the ionomycin-induced one. These results suggest that the different effects of indomethacin may be attributed to the distinct effects of 12-HETE on ZT-A- and ionomycin-induced platelet aggregations.
海洋毒素虫黄藻毒素 -A（ZT -A）和钙离子载体离子霉素可引起兔血小板聚集。虽然吲哚美辛可抑制ZT -A诱导的血小板聚集，但该药物可增强离子霉素诱导的聚集。相反，吲哚美辛可完全抑制ZT -A和离子霉素诱导的血栓素B2（TXB2，血栓素A2（TXA2）的稳定代谢产物）的积累。在吲哚美辛存在的情况下可积累的12 -羟基二十碳四烯酸（12 -HETE）可抑制ZT -A诱导的聚集，但可增强离子霉素诱导的聚集。这些结果表明，吲哚美辛的不同作用可能归因于12 -HETE对ZT -A和离子霉素诱导的血小板聚集的不同影响。
