Difference between revisions of "NSAIDs"
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NSAIDs are defined as "''agents which inhibit the formation of eicosanoids from arachidonic acid''". Prostaglandins (PGs), thromboxanes (TXs) and leukotrienes (LTs) are all eicosanoids which have an inflammatory-mediating action. | NSAIDs are defined as "''agents which inhibit the formation of eicosanoids from arachidonic acid''". Prostaglandins (PGs), thromboxanes (TXs) and leukotrienes (LTs) are all eicosanoids which have an inflammatory-mediating action. | ||
| − | Chemical or physical injury to cells causes induction of the enzyme phospholipase-A2 (PLA2), which converts phospholipids to arachidonate. This newly-formed arachidonic acid is converted by the action of cyclo-oxgygenase (COX) enzymes to cyclic endoperoxidases, which can form inflammatory mediators including PGI2, PGD2, PGE2 and TXA2. | + | Chemical or physical injury to cells causes induction of the enzyme phospholipase-A2 (PLA2), which converts phospholipids to arachidonate. This newly-formed arachidonic acid is converted by the action of cyclo-oxgygenase (COX) enzymes to cyclic endoperoxidases, which can form inflammatory mediators including PGI2, PGD2, PGE2 and TXA2. Arachidonte may also be converted to 5-HPETE to eventually form leukotrienes, and some newer NSAIDs target this branch of the pathway. |
| + | |||
| + | NSAIDs interfere with the formation of inflammatory mediators by inhibiting the action of the enzyme cyclo-oxygenase. Two forms of the enzyme exist: COX-1, which is constitutively expressed, and COX-2, which is inducible and produced by inflammatory cells. To minimise the potential for side-effects of using NSAIDs for anti-inflammatory purposes it would be ideal to target COX-2 only, leaving the "housekeeping" functions of COX-1 intact. However, most NSAIDs are non-selective COX inhibitors. | ||
==Spectrum of Activity== | ==Spectrum of Activity== | ||
Revision as of 18:21, 27 January 2009
The term "NSAIDs" stands for non-steroidal anti-inflammatory drugs. They were originially obtained from plant extracts such as willow bark, which contain agents known as salicylates. Aspirin was synthesised for the first time in 1893, and in 1972 the mode of NSAID action was discovered to be associated with cyclo-oxygenase inhibition.
Mechanism of Action
NSAIDs are defined as "agents which inhibit the formation of eicosanoids from arachidonic acid". Prostaglandins (PGs), thromboxanes (TXs) and leukotrienes (LTs) are all eicosanoids which have an inflammatory-mediating action.
Chemical or physical injury to cells causes induction of the enzyme phospholipase-A2 (PLA2), which converts phospholipids to arachidonate. This newly-formed arachidonic acid is converted by the action of cyclo-oxgygenase (COX) enzymes to cyclic endoperoxidases, which can form inflammatory mediators including PGI2, PGD2, PGE2 and TXA2. Arachidonte may also be converted to 5-HPETE to eventually form leukotrienes, and some newer NSAIDs target this branch of the pathway.
NSAIDs interfere with the formation of inflammatory mediators by inhibiting the action of the enzyme cyclo-oxygenase. Two forms of the enzyme exist: COX-1, which is constitutively expressed, and COX-2, which is inducible and produced by inflammatory cells. To minimise the potential for side-effects of using NSAIDs for anti-inflammatory purposes it would be ideal to target COX-2 only, leaving the "housekeeping" functions of COX-1 intact. However, most NSAIDs are non-selective COX inhibitors.