Anti-inflammatory effects of aspirin and sodium salicylate.

  title={Anti-inflammatory effects of aspirin and sodium salicylate.},
  author={Rainer Amann and Bernhard A. Peskar},
  journal={European journal of pharmacology},
  volume={447 1},

Therapeutic effects of nitric oxide-aspirin hybrid drugs

The authors focus on the analgesic, anti-inflammatory, cardiovascular and chemopreventative actions of compounds of this emerging drug class, known as nitric oxide (NO)-aspirins.

A novel mechanism for the anticancer activity of aspirin and salicylates

It is proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation, which may have implications in understanding the inhibitory effect of aspirin and salicylates on wound healing, given the critical role of EGF in the response to tissue trauma.

Anticancer and Anti-Inflammatory Mechanisms of NOSH-Aspirin and Its Biological Effects

This review focuses on the biological effects of NOSH-Aspirin and provides a comprehensive analysis to elucidate the mechanism underlying its disease-protective benefits.

Synthesis, acute toxicity and anti-inflammatory effect of bornyl salicylate, a salicylic acid derivative

Data suggest that BS has an anti-inflammatory effect, which is related, at least in part, with decrease of mediators as PGE2, NO and pro-inflammatory cytokines, however, further studies should be done to explore its potential as anAnti-inflammatory drug.

Acetylsalicylic acid: Incoming 150 years of the first synthesis

Acetylsalicylic acid is one of the most fascinating and versatile drugs known to medicine, as well as one of the oldest. Acetylsalicylic acid is a drug which is safe, with analgetic, antirheumatic,



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 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.