氯贝丁酯对人血小板激活的前列腺素依赖性和非依赖性途径的增强作用：环磷酸腺苷参与的证据。

Potentiating effects of clofibrate on prostaglandin-dependent and -independent pathways of human platelet activation: evidence for involvement of cyclic AMP.

作者信息

Witiak D T, Newman H A, Fertel R H, Feller D R

出版信息

Biochem Pharmacol. 1982 Jun 1;31(11):2125-8. doi: 10.1016/0006-2952(82)90434-8.

Abstract

Although clofibrate has been shown to inhibit platelet aggregation that is caused by thrombin, ADP and epinephrine, by blocking the release of arachidonic acid from platelet phospholipids [8], here we have demonstrated that clofibrate enhanced platelet aggregation by arachidonic acid and PLC and reversed the effects of PGE1 on platelet cAMP concentration and on PLC-induced secretion of [14C]-5HT in similar, concentration-dependent manners. Taken together, these findings strongly suggest that the proaggregatory effect of clofibrate is mediated by a lowering of cAMP in platelets.

摘要

尽管已表明氯贝丁酯可通过阻断血小板磷脂中花生四烯酸的释放来抑制由凝血酶、二磷酸腺苷（ADP）和肾上腺素引起的血小板聚集[8]，但我们在此证明，氯贝丁酯可通过花生四烯酸和磷脂酶C（PLC）增强血小板聚集，并以类似的浓度依赖性方式逆转前列腺素E1（PGE1）对血小板环磷酸腺苷（cAMP）浓度以及对PLC诱导的[14C] - 5羟色胺（5HT）分泌的影响。综上所述，这些发现有力地表明，氯贝丁酯的促聚集作用是由血小板中cAMP水平降低介导的。