Inhibitors of cyclooxygenase-2-dependent modulation of functional characteristics of leukocytes

Abstract

Cyclooxygenase (COX), the primary enzyme responsible for the synthesis of prostanoids, exists in at least 2 isoforms. COX-2 has been suggested to be the isoform primarily responsible for synthesis of prostaglandins (PGs) in the context of inflammation. Thus, selective inhibitors of COX-2 were developed with the aim that they would be as effective as traditional nonsteroidal antiinflammatory drugs (NSAIDs) but would not be as damaging to the gastrointestinal tract by virtue of not inhibiting the primarily COX-1-dependent PG synthesis in those tissues. To investigate whether selective COX 2 inhibitors would play a role in a model of inflammation. The received results testify to ability of COX 2 inhibitors to increase adhesion and modulation of apoptosis and PMN free oxygen radicals production. The drugs' effect on PMN free oxygen radicals production, apoptosis and adhesion may constitute an additional mechanism of their activity. These data characterize the potential mechanism to explain effects immunomodulatory agents of pathway and therapy for inflammation, cardiovascular diseases and bronchial asthma; beta-adrenergic receptors are functionally coupled to signalling cascades in human neutrophils
These results clearly confirmed that COX-2 plays a critical role in the development of the inflammatory response by altering key components of the inflammatory cascade. Therefore, selective inhibitor of COX-2 such as celecoxib, offers a therapeutic approach for the management of various inflammatory diseases.