Aspirin triggers formation of anti-inflammatory mediators: New mechanism for an old drug.
Extract: Aspirin is a widely used non-steroidal anti-inflammatory drug (NSAID). It is well documented that aspirin irreversibly inhibits cyclooxygenase (COX) by acetylation of an amino acid serine residue, and thus blocks the subsequent biosynthesis of prostaglandins and thromboxane. COX has at least two forms, COX-1 and COX-2. COX-1 is the main form present in mature platelets in the blood, where it transforms arachidonic acid to the intermediates PG-G/H, which are subsequently converted to thromboxane A2. Thromboxane A2 is a vasoconstrictor and potent platelet activator. Thus, inhibition of thromboxane A2 formation explains aspirin's anti-thrombotic properties. In the early 1990s, a second form of COX was identified, namely COX-2. COX-2 was initially conceptualized as an "inducible" COX that is elevated in its quantity by a wide range of agents that stimulate inflammation or cell division and seems to be responsible for local formation during inflammation and cancer.
Chiang
Nan
N
Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA.
Serhan
Charles N
CN