THE ROLE OF PLATELET CYCLOOXYGENASE AND LIPOXYGENASE PATHWAYS IN TUMOR-CELL INDUCED PLATELET-AGGREGATION
THE ROLE OF PLATELET CYCLOOXYGENASE AND LIPOXYGENASE PATHWAYS IN TUMOR-CELL INDUCED PLATELET-AGGREGATION
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DOI：
10.1016/0006-291x(87)91333-7
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发表时间：
1987-05-29
影响因子：
3.1
通讯作者：
SLOANE, BF
中科院分区：
文献类型：
--
作者：
HONN, KV;STEINERT, BW;SLOANE, BF
步行者256癌肉瘤细胞诱导大鼠血小板聚集并伴随产生类花生酸代谢物（例如，12-羟基二十碳四烯酸，血栓烷A2）。环氧合酶抑制剂，而不是脂氧合酶抑制剂，能够抑制体外诱导的血小板聚集低浓度的激动剂。在高激动剂浓度下，环氧合酶和脂氧合酶抑制剂均不影响血小板聚集;然而，两种抑制剂的组合导致对聚集的抑制。此外，低浓度的激动剂诱导最小的类花生酸代谢，而高浓度导致类花生酸代谢增加。这些抑制剂在测试剂量下不抑制蛋白激酶C活性。
Walker 256 carcinosarcoma cells induce the aggregation of rat platelets and concomitant production of eicosanoid metabolites (e.g., 12-hydroxyeicosatetraenoic acid, thromboxane A2). Cyclooxygenase inhibitors, but not lipoxygenase inhibitors, were able to inhibit platelet aggregation induced in vitro by low concentrations of agonists. At high agonist concentrations, neither cyclooxygenase nor lipoxygenase inhibitors affected platelet aggregation; however the combination of both inhibitors resulted in inhibition of aggregation. Also, a low concentration of agonist induced minimal eicosanoid metabolism, whereas a high concentration resulted in increased eicosanoid metabolism. These inhibitors, at the doses tested, did not inhibit protein kinase C activity.