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At least 1,279 records · Page 71Linked to original sources
PubMed2005

COX-2 inhibitors and metabolism of essential fatty acids.

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.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Can COX-2 inhibitor-induced increase in cardiovascular disease risk be modified by essential fatty acids?

Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke. This has been attributed to their ability to inhibit endothelial COX-2 derived prostacyclin (PGI2) but not platelet COX-1 derived thromboxane A2 (TXA2). On the other hand, aspirin blocks both COX-1 and COX-2 enzymes without decreasing PGI2 but blocks TXA2 synthesis that explains its beneficial action in the prevention of coronary heart disease (CHD). The inhibitory action of aspirin on COX-1 and COX-2 enzymes enhances the tissue concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). These fatty acids form precursors to PGE1, PGI2, PGI3, lipoxins (LXs), and resolvins that have anti-inflammatory actions. In contrast, increase in the concentrations of DGLA, AA, EPA, and DHA is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway. COX-2 inhibitors interfere with the formation of LXs and resolvins that have neuroprotective and cardioprotective actions. EPA and PGI2 have anti-arrhythmic action. EPA, DHA, and AA augment eNO formation that prevents atherosclerosis. This suggests that COX-2 inhibitors increase cardiovascular and stroke risk by interfering with the formation of eNO, PGI2, LXs, and resolvins and implies that combining EFAs with COX-2 inhibitors could prevent these complications.

Cardiovascular Diseases↗
PubMedDate not supplied

[The effect of alimentary hypercholesterolemia on the level of lipids and essential fatty acids in rabbit enterohepatic circulation].

Patterns of lipid metabolism were estimated in biological fluids and tissues involved in enterohepatic circulation of bile lipid complexes in female rabbits with alimentary hypercholesterolemia. Cholesterol gallstones were not found in gallbladder of rabbits with alimentary hypercholesterolemia. A number of reasons was responsible for the phenomenon, including specific ratio of four lipid components, which contributed to maintaining bile cholesterol in soluble form: concentration of bile acids was unaltered simultaneously with high contents of cholesterol and a decrease in phospholipids level, while content of free fatty acids was increased and the content of arachidonic acid was elevated in majority of lipid fractions.

Animals↗
PubMed1990

Essential fatty acid deficiency: probing the role of arachidonate in biology.

EFA deficiency appears to be a uniquely useful tool in probing the role of arachidonate in a variety of physiologic and pathologic processes. Recent studies have clarified the effects of the deficiency state on tissue fatty acid content and on the production of metabolites of arachidonate and related mediators such as PAF. The ability of EFA deficiency to ameliorate a variety of inflammatory states, particularly models of autoimmune disease, is striking. The central mechanism appears to be the ability of EFA deficiency to inhibit leukocyte migration into foci of inflammation. The mechanisms underlying this phenomenon are currently under investigation. Additionally EFA deficiency has the capacity to alter dramatically tissue immunogenicity by affecting the representation of Ia-bearing cells within tissues. The role of arachidonate in the regulation of Ia-bearing cells within tissues is an area of continuing interest.

Animals↗