Anti-inflammatories

NSAIDs are very widely used in almost all the departments of medicine. By some estimates, each year in the world more than 60 million prescriptions of non-aspirin NSAIDs are being produced. However, the actual number of patients taking NSAIDs is much more, since this medication is approved for use as a non-prescription medicines.
The action of NSAIDs at the cellular level is associated with the inhibition of the enzyme cyclooxygenase-2 (COX-2), which leads to disruption of the synthesis of prostaglandins (PG) – proinflammatory cytokines.

Anti-inflammatory effect is manifested at weakening stage of exudation (edema) and proliferation (proliferation of connective tissue). Violation of PG synthesis leads to a decrease of the selection of biologically active substances that activate inflammation (histamine, serotonin), increase membrane permeability and increase swelling. Reduction of edema happens due to the normalization of the vascular permeability of membranes during inflammation. Important role in the anti-inflammatory effect of NSAIDs is played by their antioxidants whose main property is to inhibit lipid peroxidation (LPO), the products of which are the free radicals that damage biological membranestion, therefore contributing to the progression of inflammation.

NSAIDs have a broad spectrum of side effects, including the three major groups: NSAID-induced gastropathy, drug damaged articular cartilage, and cardiovascular complications. The greatest number of side effects is associated with disorders of the gastrointestinal tract. Minimal (but not eliminated) risk of side effects on the gastrointestinal tract is caused by preferential and selective COX-2 blockers, which requires a combination of them with a proton pump blockers (omeprazole and others).