Diclofenac: Difference between revisions
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Diclofenac is believed to work by decreasing the production of [[prostaglandins]], like other drugs in this class. | Diclofenac is believed to work by decreasing the production of [[prostaglandins]], like other drugs in this class. | ||
As with most NSAIDs, the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis through [[cycloxygenase]] inhibition. Diclofenac inhibits COX-1 and COX-2 with relative equipotency.<ref name="a42">PMID:8265610</ref> | |||
The main target in inhibition of prostaglandin synthesis appears to be the transiently expressed prostaglandin-endoperoxide synthase-2 (PGES-2) also known as cycloxygenase-2 (COX-2). | |||
It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.<ref name="a43">PMID:10773497</ref> | |||
Diclofenac has a relatively high lipid solubility, making it one of the few NSAIDs that are able to enter the brain by crossing the blood-brain barrier. In the brain, too, it is thought to exert its effect through inhibition of COX-2.<ref name="a43">PMID:25078485</ref> In addition, it may have effects inside the spinal cord.<ref name="a43">PMID:27014880</ref>. | |||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||