COX-2 inhibitors and metabolism of essential fatty acids.

摘要: Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke that is attributed to their ability inhibit prostacyclin (PGI2), lipoxins, resolvins, endothelial nitric oxide (eNO) but not platelet COX-1 derived thromboxane A2 (TXA2). In contrast, aspirin blocks both enzymes that, in turn, increases intracellular concentrations dihomo-gamma-linolenic acid (DGLA), arachidonic (AA), eicosapentaenoic (EPA) docosahexaenoic (DHA) reduced formation eicosanoids. On other hand, such an much less with specific since they do block eicosanoids through pathway. DGLA, AA EPA form precursors PGE1, PGI2, PGI3 respectively, which are potent vasodilators anti-aggregators, thus aid prevention thrombus formation. has anti-arrhythmic action, EPA, DHA (docosahexaenoic acid), PGE1 have anti-inflammatory actions as well. DHA, augment eNO anti-atherosclerotic action. Hence, combining EFAs will prevent thrombotic cardiovascular events.