Aspirin, also known as acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug NSAID that is commonly used to alleviate pain, reduce inflammation, and lower fever. It exerts its therapeutic effects by inhibiting the cyclooxygenase COX enzymes, specifically COX-1 and COX-2, which play a crucial role in the synthesis of prostaglandins.Prostaglandins are hormone-like substances that are involved in various physiological processes, including inflammation, pain sensation, and regulation of body temperature. They are synthesized from arachidonic acid, a polyunsaturated fatty acid, through a series of enzymatic reactions catalyzed by the COX enzymes.There are two main isoforms of COX enzymes: COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and is responsible for maintaining the normal physiological functions of prostaglandins, such as protecting the gastric mucosa and regulating platelet aggregation. On the other hand, COX-2 is primarily induced during inflammation and is responsible for the synthesis of prostaglandins that mediate pain, fever, and inflammation.Aspirin exerts its anti-inflammatory, analgesic, and antipyretic effects by inhibiting both COX-1 and COX-2 enzymes. It does so by irreversibly acetylating a serine residue Ser-530 in COX-1 and Ser-516 in COX-2 located within the active site of the enzymes. This acetylation leads to a conformational change in the enzyme structure, which in turn prevents the binding of arachidonic acid to the active site. As a result, the conversion of arachidonic acid to prostaglandin H2 PGH2 , the precursor of other prostaglandins, is blocked, ultimately leading to a decrease in the production of prostaglandins involved in inflammation, pain, and fever.In addition to its anti-inflammatory effects, aspirin also has antithrombotic properties due to its ability to inhibit COX-1-mediated synthesis of thromboxane A2 TXA2 in platelets. TXA2 is a potent vasoconstrictor and platelet aggregator, and its inhibition by aspirin results in reduced platelet aggregation and decreased risk of blood clot formation.In summary, aspirin interacts with COX-1 and COX-2 enzymes by acetylating a serine residue within their active sites, which leads to the inhibition of prostaglandin synthesis. This, in turn, results in reduced inflammation, pain, and fever, as well as decreased platelet aggregation and blood clot formation.