通过提高环磷酸腺苷（cAMP）水平的药物抑制乙醇诱导的血小板活化。

Inhibition of ethanol-induced platelet activation by agents that elevate cAMP.

作者信息

Rubin R, Hoek J B

机构信息

Department of Pathology and Cell Biology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.

出版信息

Thromb Res. 1990 Jun 15;58(6):625-32. doi: 10.1016/0049-3848(90)90308-y.

DOI:10.1016/0049-3848(90)90308-y

PMID:2166973

Abstract

Ethanol activates phosphoinositide-specific phospholipase C in human platelets resulting in the mobilization of intracellular calcium and shape change (Arch. Biochem. Biophys. 260, 480-492, 1988). Preincubation of platelets with agents that increase levels of cAMP (i.e., forskolin, prostacyclin) inhibited these responses to ethanol in a concentration- and time-dependent manner. The inhibitory effect was potentiated by the phosphodiesterase inhibitor, isomethybutylxanthine. When added after ethanol, these agents also reversed platelet shape change and lowered cytosolic free calcium to basal levels. The results demonstrate a direct inhibitory effect of cAMP on the ethanol-induced activation of phospholipase C.

摘要

乙醇可激活人血小板中的磷酸肌醇特异性磷脂酶C，导致细胞内钙的动员和形状改变（《生物化学与生物物理学文献》260, 480 - 492, 1988）。用增加cAMP水平的试剂（即福斯高林、前列环素）预孵育血小板，可浓度和时间依赖性地抑制对乙醇的这些反应。磷酸二酯酶抑制剂异丁基甲基黄嘌呤可增强这种抑制作用。当在乙醇后添加这些试剂时，它们还可逆转血小板形状改变并将胞质游离钙降低至基础水平。结果表明cAMP对乙醇诱导的磷脂酶C激活具有直接抑制作用。