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Inhibition of nitric oxide synthesis in mouse macrophage cells by feverfew supercritical extract

Anat Aviram1, Nikolaos M Tsoukias, Steven J Melnick

  • 1Miami Children's Hospital, Department of Pathology, Miami, FL 33155, USA.

Phytotherapy Research : PTR
|September 20, 2011
PubMed

Insights

Feverfew extract effectively reduces migraine-associated inflammation by inhibiting nitric oxide (NO) and TNF-α production. This mechanism involves down-regulating specific enzyme proteins, not their genetic material.

Area of Science:

  • Pharmacology
  • Immunology
  • Herbal Medicine

Background:

  • Feverfew (Tanacetum parthenium) is a widely recognized herbal remedy for migraine headaches.
  • Understanding its anti-migraine mechanisms requires investigation at the cellular level.

Purpose of the Study:

  • To elucidate the in vitro antimigraine mechanism of feverfew supercritical extract.
  • To investigate the impact of feverfew on inflammatory mediators in a cellular model.

Main Methods:

  • Utilized the mouse macrophage cell line (RAW 264.7) treated with lipopolysaccharide.
  • Quantified nitric oxide (NO) and TNF-α synthesis using ELISA.
  • Analyzed gene and protein expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) via RT-PCR and Western blot.

Main Results:

  • Feverfew extract demonstrated dose-dependent inhibition of NO and TNF-α production.
  • Complete inhibition of NO was observed at 5 µg/mL of feverfew extract.
  • While mRNA levels of eNOS and iNOS remained unchanged, their protein expression was significantly down-regulated.

Conclusions:

  • Feverfew's inhibition of NO synthesis is attributed to the down-regulation of eNOS and iNOS enzymes.
  • This regulation occurs at the translational and/or post-translational levels, impacting protein expression rather than gene transcription.

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