Key result
Aspirin and indomethacin, but not BW755C, directly inhibited collagen-induced arachidonic acid liberation from phosphatidylcholine and phosphatidylinositol in human platelets.
Aspirin and indomethacin directly inhibit collagen-induced arachidonic acid liberation from phosphatidylcholine and phosphatidylinositol in human platelets, independent of cyclo-oxygenase metabolites.
Answers are grounded in this paper and cite their sources.
May indicate COX-independent platelet effects of aspirin; leaves open in vivo relevance and clinical translation.
Stimulation of platelets with collagen results in the mobilization of arachidonic acid (AA) from phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylserine (PS) and phosphatidylinositol (PI). In this study the effect of aspirin, indomethacin, BW755C and prostaglandin H2 (PGH2) on labelled AA release in response to varied concentrations of collagen was investigated. Our results indicate that aspirin (0.56 mM) and indomethacin (5.6 microM) not only inhibited the collagen-mediated formation of cyclo-oxygenase metabolites, but also caused a significant reduction in the accumulation of free labelled AA and 12-hydroxyeicosatetraenoic acid (12-HETE) (21-64%). Aspirin and indomethacin also inhibited the release of [3H]AA from PC (37-75%) and PI (33-63%). The inhibition of AA release caused by aspirin was reversed partially by PGH2 (1 microM). In contrast, a smaller/no inhibition of collagen-stimulated labelled AA and 12-HETE accumulation (0-11%) and of collagen-stimulated AA loss from PC and PI was observed in the presence of BW755C. The results obtained in the presence of aspirin, indomethacin and BW755C at lower concentrations of collagen further demonstrate that AA release from PI (45-61% inhibition at 10 micrograms of collagen), but not from PC, was affected by the inhibition of cyclo-oxygenase. The results obtained on the effect of PGH2 further support that deacylation of phospholipids occurs independently of cyclo-oxygenase metabolites, particularly at higher concentrations of collagen. These results also demonstrate that aspirin and indomethacin, but not BW755C, cause a direct inhibition of collagen-induced [3H]AA liberation from PC as well as from PI. We also conclude that the diacylglycerol lipase pathway is a minor, but important, route for AA release from PI in collagen-stimulated human platelets. The mechanisms underlying the regulation of AA release by collagen in the absence of cyclo-oxygenase metabolites are not clear.
No takes yet. Share an insight, caveat, or question.
Vedelago et al. (1988) studied this question. Aspirin, indomethacin, BW755C, and PGH2 was evaluated on Arachidonic acid release and 12-HETE accumulation. Aspirin and indomethacin, but not BW755C, directly inhibited collagen-induced arachidonic acid liberation from phosphatidylcholine and phosphatidylinositol in human platelets.
Synapse has enriched 10 related papers. Consider them for comparative context: