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.
tieecaApnonhm cats yb hbinniigti the O-XC3 in eth SCN adn eehcn eisnearcgd het obyd t,rrmeaeeupt utb nto no teh pplieerhra XO1C- pa;&m .2 ne,ehc snpAiir is eth betert cchoei
submitted by โlfsuarez(160)
It can be re-accessed by making a purchase.
Purchase your membership here
$279$49 65% OFFhneW tsintape aer ingev iiotcnNic (diNc)aainic htey era dtlo to petecx ocomnm sdie sefcfte to ucroc hcsu as tawrhm nda rsedn.se eOn can avoid eesht edis cetfsfe yb kgtnai snaiipr
$279$49 65% OFF