In the presence of inflammatory states, the main objectives of the drug therapy of inflammation are to limit and preferably eliminate the typical symptoms (such as, for example, pain) and to slow down or, even better, stop the tissue damage that inevitably follows.
The substances and chemical mediators involved in that complex process that is inflammation are many. A determining role is certainly played by some particular types of prostaglandins. It is therefore not surprising that the target of NSAIDs is precisely an enzyme - cyclooxygenase or COX. - involved in the synthetic process of prostaglandins starting from arachidonic acid.
polyunsaturated which are synthesized in different tissues and play multiple roles in the organism.
Belonging to the group of eicosanoids, prostaglandins are involved both in physiological processes (cellular homeostasis) and in inflammatory processes.
Although prostaglandins can be synthesized from different types of polyunsaturated fatty acids, only those from arachidonic acid will be considered in this article. Starting from the latter, through the action of a particular enzyme called cyclooxygenase (COX), it is possible to synthesize prostaglandins G2, H2, E2, F2α, D2, I2 and thromboxane A2.
Three isoforms are currently known of the cyclooxygenase enzyme:
- COX-1: is the constitutive isoform normally expressed in cells and involved in their homeostasis.
- COX-2: it is an inducible isoform, which means that it is not always functional inside the cells but is activated only following tissue damage; it is responsible for the synthesis of the so-called pro-inflammatory prostaglandins.
- COX-3: This isoform is believed to be centrally located, although many of its features and functions remain currently misunderstood.
