Cyclooxygenase-1 and Cyclooxygenase-2 Knockout Mice Provide Insights into Beneficial and Adverse Effects of Nonsteroidal Anti-Inflammatory Drugs

Author(s):  
Robert Langenbach
2001 ◽  
Vol 53 (12) ◽  
pp. 1679-1685 ◽  
Author(s):  
Miyako Kato ◽  
Shinichi Nishida ◽  
Hidero Kitasato ◽  
Natsue Sakata ◽  
Shinichi Kawai

2018 ◽  
Vol 3 (3) ◽  
pp. 270
Author(s):  
Vinay Kumar ◽  
Lilly Ganju ◽  
Iti Garg

<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>


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