scholarly journals Role of Cyclooxygenase Pathway and Risk Associated with Non-Steroidal Anti-inflammatory Drugs Therapy in Cardiovascular Diseases

2018 ◽  
Vol 3 (3) ◽  
pp. 270
Author(s):  
Vinay Kumar ◽  
Lilly Ganju ◽  
Iti Garg
Keyword(s):  
Vascular Wall ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase 2 ◽  
Cardiovascular Risks ◽  
Membrane Phospholipids ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Prostacyclin Production

<p>Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase enzyme activity through different<br />mechanisms and prevent inflammation. But they all have different risks associated with them. Some are associated with<br />gastrointestinal bleeding and some are strongly allied with the cardiovascular risks. Cyclooxygenase enzyme regulates<br />prostaglandin synthesis by converting arachidonic acid present at the sn-2 position of membrane phospholipids to<br />prostaglandin H2. Prostaglandin H2 is the precursor of all prostaglandins. There are two isoforms of cyclooxygenase<br />enzyme, cyclooxygenase-1 and cyclooxygenase-2 which differ in their active site due to an isoleucine to valine<br />substitution at amino acid 523 in cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed in platelets<br />where it helps in the formation of thromboxane whereas cyclooxygenase-2 is inductive form and is expressed in<br />the endothelial cells due to shear stress and forms prostacyclins. Both thromboxanes and prostacyclins maintain<br />the homeostasis of the vascular wall. During vascular injury prostacyclin production decreases as a result of which<br />thromboxane synthesis increases in the platelets which leads to platelet aggregation. Although, being strongly<br />associated with cardiovascular risks, NSAIDs are still prescribed to the patients to prevent pain according to their<br />condition. So this review aims to summarise the mechanism of cyclooxygenase pathway, possible mechanism of<br />action of NSAIDs and the risks of cardiovascular events associated with the use of NSAIDs.</p>

The role of celecoxib as a potential inhibitor in the treatment of inflammatory diseases - a review

2021 ◽  
Vol 28 ◽  
Author(s):  
Josiane Viana Cruz ◽  
Joaquín María Campos Rosa ◽  
Njogu Mark Kimani ◽  
Silvana Giuliatti ◽  
Cleydson Breno Rodrigues dos Santos
Keyword(s):  
Side Effects ◽  
Inflammatory Diseases ◽  
Structural Basis ◽  
Potential Inhibitor ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Cox 2 Inhibitors

: This article presents a simplified view of celecoxib as a potential inhibitor in the treatment of inflammatory diseases. The enzyme cyclooxygenase (COX) has, predominantly, two isoforms called cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). The former plays a constitutive role that is related to homeostatic effects in renal and platelets, while the latter is mainly responsible for induction of inflammatory effects. Since COX-2 plays an important role in the pathogenesis of inflammatory diseases, it has been signaled as a target for the planning of anti-inflammatory intermediates. Many inhibitors developed and planned for COX-2 inhibition have presented side effects to humans, mainly in the gastrointestinal and/or cardiovascular tract. Therefore, it is necessary to design new potential COX-2 inhibitors, which are relatively safe and without side effects. To this end, of the generation of non-steroidal anti-inflammatory drugs from “coxibs”, celecoxib is the only potent selective COX-2 inhibitor that is still commercially available. Thus, the compound celecoxib became a commercial prototype inhibitor for the development of anti-inflammatory agents for COX-2 enzyme. In this review, we provide highlights where such inhibition should provide a structural basis for the design of promising new non-steroidal anti-inflammatory drugs (NSAIDs) which act as COX-2 inhibitors with lesser side effects on the human body.

Cyclooxygenase-1 and cyclooxygenase-2 selectivity of non-steroidal anti-inflammatory drugs: investigation using human peripheral monocytes

2001 ◽  
Vol 53 (12) ◽  
pp. 1679-1685 ◽  
Author(s):  
Miyako Kato ◽  
Shinichi Nishida ◽  
Hidero Kitasato ◽  
Natsue Sakata ◽  
Shinichi Kawai
Keyword(s):  
Cyclooxygenase 2 ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

ROLE OF PROSTAGLANDINS IN THE CONTROL OF THE FUNCTION OF ADRENAL GLOMERULOSA CELLS

1981 ◽  
Vol 91 (3) ◽  
pp. 427-437 ◽  
Author(s):  
P. ENYEDI ◽  
A. SPÄT ◽  
F. A. ANTONI
Keyword(s):  
Arachidonic Acid ◽  
Production Rate ◽  
Prostaglandin Synthesis ◽  
Competitive Antagonist ◽  
Aldosterone Production ◽  
Prostaglandin F ◽  
Inflammatory Drugs ◽  
Glomerulosa Cells ◽  
Anti Inflammatory

The role of prostaglandins in the control of aldosterone production was studied in isolated rat glomerulosa cells. Exogenous prostaglandin E2 in concentrations above 10−9 mol/l increased the production rate of aldosterone; this effect was attenuated by the competitive antagonist, 7-oxa-13-prostynoic acid. Prostaglandin F2α (10−9–10−5 mol/l) failed to influence the production rate of aldosterone. The aldosterone-stimulating effect of the prostaglandin precursor, arachidonic acid (5 × 10−4 mol/l), could not be blocked by inhibitors of prostaglandin synthesis. Basal production rate of aldosterone was not significantly influenced by non-steroidal anti-inflammatory drugs. Glomerulosa cells were stimulated by angiotensin II; this effect was not potentiated by arachidonic acid and was reduced only slightly by indomethacin. The cells were also stimulated by corticotrophin and potassium ions. The effect of these substances was not potentiated by arachidonic acid and was not inhibited by non-steroidal anti-inflammatory drugs. These results do not confirm the presumption that intra-adrenal prostaglandins play an essential role in the control of aldosterone secretion. Some effects of arachidonic acid and its antagonist, eicosatetraynoic acid, on aldosterone production are considered to be independent of changes in prostaglandin synthesis.

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