NSAIDs act through inhibition of cyclooxygenase enzyme (COX-1 and COX-2), thus inhibiting prostaglandin synthesis. Arachidonic acid is a polyunsaturated fatty acid that is metabolised into prostaglandins (G2, H2) and prostanoids (E2, D2, F2α, I2 and thromboxane A2). Prostanoids act via cell membrane receptors. Phospholipase A2 metabolises arachidonic acid into prostaglandins. CPLA2α is the main subform of cytosolic enzyme involved in the release of arachidonic acid. COX enzyme has three domains. One of the domains is catalytic and has two active sites. Arachidonic acid is metabolised by catalytic domain to PGG2. COX-1 is a constitutive enzyme as it is expressed during the whole life of the cell. It is involved with function of the platelets, GI tract and renal system. COX-2 has a shorter half-life and is expressed during inflammation. IL-β is upregulated at the site of inflammation and is a major inducer of COX-2. The induction of COX-2 occurs both at the peripheral level and at the central nervous system. COX-1 is present in the endoplasmic reticulum and nuclear membrane whereas COX-2 is present only in the nuclear membrane.