Abstract
Aspirin [acetylsalicylic acid (ASA)] is the lead nonsteroidal drug (NSAID) and is widely used to relieve inflammation.1, 2 Recent results indicate that its use in low doses is also associated with new, previously unappreciated beneficial effects, including reduced risk of heart disease3 and decreased incidence of lung, colon and breast cancer,4 and in vitro it can inhibit nuclear factor-κB transcription, which may be relevant in treatment of patients with human immunodeficiency virus.5 ASA’s target is the cyclooxygenase activity of prostaglandin G/H synthase (PGHS). It does not inhibit the lipoxygenases (LOs).6-8 Although blockage of PGs and TXs can account for many of ASA’s pharmacologic properties, the mechanism of action of this important drug in several clinical settings including lowering the risk of human cancer is still a subject of interest and debate. 1, 2
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Serhan, C.N., Clària, J. (1996). Aspirin Switches Biosynthetic Circuits Triggering Novel Eicosanoids during Cell-Cell Interactions that Are Potent Inhibitors of Neutrophil Migration and Tumor Cell Proliferation. In: Vanderhoek, J.Y. (eds) Frontiers in Bioactive Lipids. GWUMC Department of Biochemistry and Molecular Biology Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5875-0_20
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DOI: https://doi.org/10.1007/978-1-4615-5875-0_20
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