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Naproxen, a common pain reliever, lowers essential tryptophan levels by displacing it, not by inhibiting Cox enzymes. Tryptophan supplementation in mice counteracted naproxen

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Area of Science:

  • Pharmacology
  • Biochemistry
  • Immunology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) alleviate pain and inflammation but pose risks to the gastrointestinal and cardiovascular systems.
  • Traditional NSAIDs and selective cyclooxygenase-2 (COX-2) inhibitors like celecoxib have different safety profiles.
  • Tryptophan metabolism is crucial for immune function and has implications for mood disorders.

Purpose of the Study:

  • To compare the effects of naproxen and celecoxib on tryptophan metabolism in humans and mice.
  • To elucidate the mechanism by which naproxen affects tryptophan levels.
  • To investigate whether tryptophan supplementation can mitigate naproxen-induced side effects.

Main Methods:

  • Human volunteers received naproxen or celecoxib, with plasma levels of tryptophan and kynurenine measured.
  • Studies were replicated in mice to validate human findings.
  • Experiments were conducted to differentiate between COX inhibition and direct displacement as mechanisms for tryptophan reduction.
  • Mice treated with naproxen received tryptophan supplementation to assess its protective effects.

Main Results:

  • Naproxen treatment led to decreased plasma tryptophan and kynurenine levels in humans and mice.
  • The reduction in tryptophan was attributed to naproxen displacing bound tryptophan, independent of COX-1 or COX-2 inhibition.
  • Tryptophan supplementation in naproxen-treated mice ameliorated fecal blood loss and reduced IL-1β-driven inflammatory gene expression in the heart.

Conclusions:

  • Naproxen's impact on tryptophan levels is primarily due to displacement, not COX inhibition.
  • Tryptophan plays a role in mitigating naproxen-induced gastrointestinal and cardiac inflammation.
  • These findings suggest a novel mechanism for NSAID-related side effects and a potential therapeutic strategy involving tryptophan.