scholarly journals Comparative Study of the Pre-emptive Analgesic Effects of Nonsteroidal Anti-inflammatory Drugs Having Different Mechanisms of Action, for Pain Associated with Extraction of Impacted Wisdom Teeth-Comparison of the Drugs Among Selective Cyclooxygenase-2 Inhibitor with/without Anti-bradykinin Effect and Cyclooxygenase-1, -2 Inhibitor-

2007 ◽  
Vol 57 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Akihide Negishi ◽  
Asuka Tsuchiya ◽  
Tomohiro Ishikita ◽  
Toru Yamaguchi ◽  
Yoshiki Nakasone ◽  
...  
Keyword(s):  
Comparative Study ◽  
Mechanisms Of Action ◽  
Cyclooxygenase 2 ◽  
Analgesic Effects ◽  
Cyclooxygenase 1 ◽  
Wisdom Teeth ◽  
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 Non-steroidal anti-inflammatory drugs dampen the cytokine and antibody response to SARS-CoV-2 infection

2021 ◽  
Author(s):  
Jennifer S. Chen ◽  
Mia Madel Alfajaro ◽  
Ryan D. Chow ◽  
Jin Wei ◽  
Renata B. Filler ◽  
...  
Keyword(s):  
Immune Response ◽  
Viral Replication ◽  
Cyclooxygenase 2 ◽  
Nsaid Treatment ◽  
Susceptibility To Infection ◽  
Cyclooxygenase 1 ◽  
Inflammatory Drugs ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Cox 1

Abstract Identifying drugs that regulate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and its symptoms has been a pressing area of investigation during the coronavirus disease 2019 (COVID-19) pandemic. Nonsteroidal anti-inflammatory drugs (NSAIDs), which are frequently used for the relief of pain and inflammation, could modulate both SARS-CoV-2 infection and the host response to the virus. NSAIDs inhibit the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which mediate the production of prostaglandins (PGs). As PGs play diverse biological roles in homeostasis and inflammatory responses, inhibiting PG production with NSAIDs could affect COVID-19 pathogenesis in multiple ways, including: (1) altering susceptibility to infection by modifying expression of angiotensin-converting enzyme 2 (ACE2), the cell entry receptor for SARS-CoV-2; (2) regulating replication of SARS-CoV-2 in host cells; and (3) modulating the immune response to SARS-CoV-2. Here, we investigate these potential roles. We demonstrate that SARS-CoV-2 infection upregulates COX-2 in diverse human cell culture and mouse systems. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication. In contrast, in a mouse model of SARS-CoV-2 infection, NSAID treatment reduced production of pro-inflammatory cytokines and impaired the humoral immune response to SARS-CoV-2 as demonstrated by reduced neutralizing antibody titers. Our findings indicate that NSAID treatment may influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies rather than modifying susceptibility to infection or viral replication. Importance Public health officials have raised concerns about the use of nonsteroidal anti-inflammatory drugs (NSAIDs) for treating symptoms of coronavirus disease 2019 (COVID-19). NSAIDs inhibit the enzymes cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), which are critical for the generation of prostaglandins – lipid molecules with diverse roles in homeostasis and inflammation. Inhibition of prostaglandin production by NSAIDs could therefore have multiple effects on COVID-19 pathogenesis. Here, we demonstrate that NSAID treatment reduced both the antibody and pro-inflammatory cytokine response to SARS-CoV-2 infection. The ability of NSAIDs to modulate the immune response to SARS-CoV-2 infection has important implications for COVID-19 pathogenesis in patients. Whether this occurs in humans and whether it is beneficial or detrimental to the host remains an important area of future investigation. This also raises the possibility that NSAIDs may alter the immune response to SARS-CoV-2 vaccination.

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