COX-2 is not involved in thromboxane biosynthesis by activated human platelets.

摘要: The occurrence of aspirin resistance has been inferred by the assessment platelet aggregation ex vivo in patients with ischemic vascular syndromes taking aspirin. Since is a weak inhibitor inducible isoform prostaglandin H synthase (COX-2), it was suggested that COX-2 may play role resistance. However cellular source(s) possibly responsible for remains unknown. Recently, expression circulating human platelets reported. To investigate possible contribution thromboxane (TX) biosynthesis, we have compared inhibitory effects NS-398 and aspirin, selective inhibitors COX-1, respectively, on prostanoid biosynthesis thrombin-stimulated vs lipopolysaccharide (LPS)stimulated monocytes (expressing high levels COX-2) isolated from whole blood healthy subjects. 180-fold more potent inhibiting monocyte activity than TXB2 production. In contrast, (55 micromol/L) largely suppressed production without affecting activity. By using specific Western blot techniques, failed to detect while COX-1 readily detectable. Our results argue against involvement TX activated consequently dispute as an important mechanism