Aspirin prevents the synthesis of prostaglandins.
Prostaglandin synthesis is the manufacture of lipid compounds within the cells of some animals, including humans. These substances are chemical messengers involved in biological processes, such as inflammation, and are important for the normal function of many different tissues. Certain enzymes initiate prostaglandin synthesis by catalyzing a series of metabolic reactions that convert a fatty acid into the final biologically active product. Medications such as aspirin prevent the synthesis of prostaglandins and thus reduce pain and inflammation.
Prostaglandin gel can be used late in pregnancy to ripen the cervix, which should stimulate labor.
In many animal tissues, prostaglandins function as cell signaling molecules that have functions ranging from signaling body temperature to the brain to sensitizing neurons to pain. These lipid compounds come in three main subtypes and together they make up the eicosanoids, a group of biologically active fatty acids. Prostaglandin synthesis occurs within cells whenever one of the compounds is needed, but they are not stored in specialized compartments as biologically important molecules usually are. With many different effects on neurons, muscles, and epithelium, prostaglandin is synthesized almost constantly in the body.
When enzymes known as cyclooxygenases (COX) are released, prostaglandin synthesis begins through the oxidation of fatty acids, primarily arachidonic acid. The fatty acids themselves come from the same sources as the lipids that make up the cell membrane. Oxidation changes its basic structure to whatever type of prostaglandin is needed at the time. COX 1 is the enzyme responsible for maintaining normal levels of prostaglandins in the body, while COX 2 mediates synthesis when tissues are injured or infected. Synthesis occurs in almost all cell types, with the exception of leukocytes and those without nuclei.
Every time tissue damage occurs, various immune cells migrate to the site. This cellular response process triggers the release of COX-2, which results in the synthesis of prostaglandins in the damaged part of the body. Prostaglandins lead to an inflammatory response, causing fever and limiting infection and tissue loss. Another variety regulates some of the blood’s clotting mechanisms, controlling where a clot can and cannot form. The prostaglandin known as PGE-2 causes changes in the uterus, including contractions, and is commonly used clinically to induce labor or abortion.
Several chemicals can inhibit prostaglandin synthesis; aspirin is a well-known example. Both COX-1 and COX-2 are inhibited by aspirin, which prevents the oxygenation of the arachidonic acid necessary for its synthesis. By preventing enzyme activity, aspirin interrupts the inflammatory pathway and reduces fever along with pain sensitivity, as both decrease without the effects of prostaglandin. Along with compounds such as ibuprofen, aspirin is one of the nonsteroidal anti-inflammatory drugs (NSAIDs). Unlike steroids like cortisone, NSAIDs prevent the production of prostaglandins instead of treating their effects.