COX-3, a splice variant of COX-1, has been suggested to be the site of action of paracetamol, but genomic and kinetic analysis indicates that this selective interaction is unlikely to be clinically relevant. There is considerable evidence that the analgesic effect of paracetamol is central and is due to activation of descending serotonergic pathways, but its primary site of action may still be inhibition of PG synthesis. The action of paracetamol at a molecular level is unclear but could be related to the production of reactive metabolites by the peroxidase function of COX-2, which could deplete glutathione, a cofactor of enzymes such as PGE synthase.
But mainly, Acetominophen is an antipyretic and analgesic, but it is not antiinflammatory, so it wouldn't be useful for Niacin induced flushing.
antpohecmieAn stac yb iinnitihgb teh -C3XO in hte CSN dna ncehe sarngdecei teh oydb rtpa,ueermte utb otn no teh lhrreieapp XOC-1 ;am&p 2. ,nehec npiriAs si het rteteb echoci
submitted by โlfsuarez(160)
It can be re-accessed by making a purchase.
Purchase your membership here
$279$49eWnh sinettpa are egivn coiNnitic d(ai)icacniN heyt era odlt ot etxpec onommc sedi sefecft to cucor uhsc sa trhmwa nad nedrse.s eOn acn viado eshet iesd csfetfe by tniagk nisarpi
$279$49