Anti-inflammatory effects of aspirin and sodium salicylate.

@article{Amann2002AntiinflammatoryEO,
  title={Anti-inflammatory effects of aspirin and sodium salicylate.},
  author={Rainer Amann and Bernhard A. Peskar},
  journal={European journal of pharmacology},
  year={2002},
  volume={447 1},
  pages={
          1-9
        }
}
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306 Citations
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306 Citations

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References

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Salicylate reverses in vitro aspirin inhibition of rat platelet and vascular prostaglandin generation.

Antiinflammatory action of salicylates: aspirin is not a prodrug for salicylate against rat carrageenin pleurisy.

Pharmacokinetics of aspirin and salicylate in relation to inhibition of arachidonate cyclooxygenase and antiinflammatory activity.

The antiinflammatory action of both drugs depends on the inhibition of PGE2 synthesis by salicylate, and aspirin was considerably more potent than saliylate in inhibiting thromboxane B2 production in clotting blood.

Salicylate-aspirin interaction in the rat. Evidence that salicylate accumulating during aspirin administration may protect vascular prostacyclin from aspirin-induced inhibition.

The interference with aspirin of its major endogenous metabolite should be borne in mind when interpreting results obtained with high dose aspirin or during repeated administration of this drug.

Sodium salicylate inhibits cyclo-oxygenase-2 activity independently of transcription factor (nuclear factor kappaB) activation: role of arachidonic acid.

Sodium salicylate is an effective inhibitor of COX-2 activity at concentrations far below those required to inhibit NF-kappaB activation and is easily displaced by arachidonic acid.

Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB.

The antiinflammatory effects of aspirin and sodium salicylate, but not glucocorticoids, are largely mediated by the antiinflammatory autacoid adenosine independently of inhibition of prostaglandin synthesis by COX-1 or COX2 or of the presence of p105.

Sodium salicylate interferes with the inhibitory effects of aspirin and indomethacin on human platelets.

Non-steroidal anti-inflammatory drugs react with two sites on platelet cyclo-oxygenase. Evidence from "in vivo" drug interaction studies in rats.

Sodium salicylate inhibits prostaglandin formation without affecting the induction of cyclooxygenase-2 by bacterial lipopolysaccharide in vivo.

It is shown that salicylate inhibits LPS-induced COX-2 activity in vivo in a manner that is overcome by provision of excess substrate and independent of effects on COx-2 expression.

Suppression of inducible cyclooxygenase 2 gene transcription by aspirin and sodium salicylate.

The findings suggest that salicylate exerts its antiinflammatory action in part by suppressing COX-2 induction, thereby reducing the synthesis of proinflammatory prostaglandins.
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