ABSTRACT
Nonsteroidal anti-inflammatory drugs (NSAIDS) are a group of drugs that inhibit cyclooxygenase and/or lipoxygenase in the metabolic pathway from arachidonic acid to the production of prostaglandins or leukotrienes [1]. Mechanisms in which these agents may decrease inflammation may involve decreasing chemotactic stimuli to leukocytes and stabilizing lysosomes so that there is decreased release of lysosomal enzymes. By inhibiting cyclooxygenase, there may be decreased production of superoxide, which can become an hydroxyl free radical. Both superoxide and hydroxyl free radicals are oxidizing agents that can easily produce tissue damage [2]. Some NSAIDS, such as indomethacin, inhibit phosphodiesterase, which produces an increase in intracellular cAMP. Increased cAMP is known to stabilize cellular lysosomal membranes and thus causes a decrease in the release of tissue-damaging lysosomal enzymes [2].
