Diclofenac: Difference between revisions
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It also may inhibit [[phospholipase A2]] as part of its mechanism of action. These additional actions may explain its high potency – it is the most potent NSAID on a broad basis.<ref name="a46">PMID:3085490</ref> <scene name='97/974935/Cv/2'>Crystal structure of the complex formed between phospholipase A2 and diclofenac</scene> ([[2b17]]). <scene name='97/974935/Binding_site/1'>Diclofenac binding site</scene>. | It also may inhibit [[phospholipase A2]] as part of its mechanism of action. These additional actions may explain its high potency – it is the most potent NSAID on a broad basis.<ref name="a46">PMID:3085490</ref> <scene name='97/974935/Cv/2'>Crystal structure of the complex formed between phospholipase A2 and diclofenac</scene> ([[2b17]]). <scene name='97/974935/Binding_site/1'>Diclofenac binding site</scene>. | ||
Besides the COX and phospholipase A2 inhibition, a number of other molecular targets of diclofenac possibly contributing to its pain-relieving actions have recently been identified. These include: | |||
*Blockage of voltage-dependent sodium channels (after activation of the channel, diclofenac inhibits its reactivation also known as phase inhibition) | |||
*Blockage of acid-sensing ion channels (ASICs)<ref name="a48">PMID:11588175</ref> | |||
*Positive allosteric modulation of KCNQ- and BK-potassium channels (diclofenac opens these channels, leading to hyperpolarization of the cell membrane) | |||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||