Experimental models used to investigate the differential inhibition of cyclooxygenase-1 and cyclooxygenase-2 by non-steroidal anti-inflammatory drugs

1998 ◽  
Vol 47 (0) ◽  
pp. 93-101 ◽  
Author(s):  
M. Pairet ◽  
J. van Ryn
Keyword(s):  
Experimental Models ◽  
Cyclooxygenase 2 ◽  
Differential Inhibition ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

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

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>

scholarly journals Differential inhibition of fracture healing by non-selective and cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs

2003 ◽  
Vol 21 (4) ◽  
pp. 670-675 ◽  
Author(s):  
Louis C. Gerstenfeld ◽  
Mark Thiede ◽  
Karen Seibert ◽  
Cindy Mielke ◽  
Deborah Phippard ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Cyclooxygenase 2 ◽  
Differential Inhibition ◽  
Inflammatory Drugs ◽  
Anti Inflammatory
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