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COX-2 inhibitors and metabolism of essential fatty acids.

Abstract：

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

journal_name

Med Sci Monit

journal_title

Medical science monitor : international medical journal of experimental and clinical research

authors

Das UN

subject

Has Abstract

pub_date

2005-07-01 00:00:00

pages

RA233-7

issue

7

eissn

1234-1010

issn

1643-3750

pii

7264

journal_volume

11

pub_type

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