Does the COX-1/COX-2 concept still hold?

Recognition that non-steroidal anti-inflammatory drugs were inhibitors of prostaglandin synthesis was critical to understanding of both their therapeutic activity and gastrointestinal pathology. In the stomach and duodenum, inhibition of prostaglandin synthesis abrogates defensive mechanisms such as mucosal blood flow, and mucus and bicarbonate secretion, and leads to the development of micro erosions that deepen ultimately to become ulcers as a consequence of acid peptic attack. Subsequently it has become clear that prostaglandin synthesis derives from two distinct but similar cyclooxygenase enzymes. The constitutive cyclooxygenase (COX)-1 is expressed in many tissues including the gastrointestinal tract. The inducible cyclooxygenase (COX)-2 becomes highly expressed under the influence of many factors such as cytokines and growth factors in tissue injury, inflammation and malignant transformation. The COX-1/COX-2 hypothesis was that drugs which inhibit COX-2 would share the therapeutic active of NSAIDs but without their adverse effects.