Aspirin and other nonsteroidal anti-inflammatory drugs (NSAID) inhibit inflammation by inhibiting an enzyme in the prostaglandin pathway, but by inhibiting this enzyme and this pathway they also inhibit pathways that protect the stomach from damage by stomach acid and that prevent aggregation of blood platelets to form blood clots. What can you conclude from this?

Aspirin works by inhibiting the production of prostaglandins. Aspirin inhibits the formation of prostaglandins by combining with the COX enzymes. Prostaglandins function as messenger molecules to monitor different physiological procedures in distinct regions of the body. One of the prime activities of prostaglandins is to stimulate inflammation and pain.

Prostaglandins are also the essential controller of platelet aggregation. By changing the COX enzymes inside the platelets, aspirin makes platelets to lose the stickiness, which is required to instigate clotting of blood.

There are two forms of cyclooxygenase, that is, COX-1 and COX-2. COX-1 generates prostaglandins and COX-2 mediates pain and swelling in response to tissue injury. Aspirin prevents both COX-1 and COX-2 functioning, while COX-2 is the therapeutic target of the drug.

However, it is the association of aspirin with COX-1 in the gastrointestinal tract, which results in the unwanted side effects of the drug. COX-1 is required to sustain a thick lining of the stomach. As aspirin inhibits the COX-1 enzyme, thus, the continuous use of the drug can result in the thinning of mucus, which safeguards the stomach from gastric juices.

In such cases, stomach bleeding, ulcers, and in certain situations perforation of the stomach can take place. Therefore, aspirin exhibits both bad and good effects.