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Review
. 2018 Jun;50(2):116-121.
doi: 10.5152/eurasianjmed.2018.0010. Epub 2018 Jun 1.

Effects of Nonsteroidal Anti-Inflammatory Drugs at the Molecular Level

Affiliations
Review

Effects of Nonsteroidal Anti-Inflammatory Drugs at the Molecular Level

Caner Gunaydin et al. Eurasian J Med. 2018 Jun.

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for their anti-inflammatory, analgesic, and antipyretic effects. NSAIDs generally work by blocking the production of prostaglandins (PGs) through the inhibition of two cyclooxygenase enzymes. PGs are key factors in many cellular processes, such as gastrointestinal cytoprotection, hemostasis and thrombosis, inflammation, renal hemodynamics, turnover of cartilage, and angiogenesis. Interest has grown in the various effects of NSAIDs during the last decade. Epidemiological studies have revealed the reduced risk of several cancer types and neurodegenerative diseases by prolonged use of NSAIDs. Recent advances in the understanding of the cellular and molecular mechanisms of NSAIDs will accelerate the processes of discovery and clinical implementation. This review summarizes the molecular mechanisms of NSAIDs on the body systems.

Keywords: Nonsteroidal anti-inflammatory drugs; cyclooxygenase; mechanism; molecular.

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Conflict of interest statement

Conflict of Interest: Authors have no conflict of interest to declare.

Figures

Figure 1.
Figure 1.
Schematic presentation of cyclooxygenase and lipoxygenase pathway PGH2: prostaglandin H2; PGF2: prostaglandin F2; PGD2: prostaglandin D2; PGE2: prostaglandin E2; PGI: prostacyclin; TXA2: thromboxane A2; PHJ2: prostaglandin J2; PGF2α: prostaglandin F2α; MMP9: matrix metalloproteinase 9; VEGF: vascular endothelial growth factor; TP: thromboxane receptor; EP1, 2, 3, and 4: prostaglandin E receptors; HUVEC: human umbilical vein endothelial cell; PPAR: peroxisome proliferator-activated receptor; PTEN: phosphatase and tensin homolog

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