An inhibitor of NF-kB might be a novel, effective, anti-migraine drug
Nuclear factor-kappaB as a molecular target for migraine therapy
Summary of the abstract
Nitric oxide (NO) generated from inducible NO synthase (iNOS) participates in immune and inflammatory responses in many tissues.
Because inflammation and iNOS are potential therapeutic targets, we examined transcriptional regulation of iNOS.
iNOS expression is preceded by significant nuclear factor kappa B (NF-kappaB) activity.
NF-kappaB activation, and iNOS expression were attenuated by parthenolide (3mg/kg), the active constituent of feverfew, an anti-inflammatory drug used for migraine treatment.
We conclude, based on results with this animal model, that blockade of NF-kappaB activity provides a novel transcriptional target for the development of anti-migraine drugs.
It’s not feverfew or parthenolide, it’s NF-kB inhibition
The authors specifically mention feverfew, and its proposed active ingredient parthenolide.
But what’s important is not the specific plant or molecule. What’s important is the inhibition of NF-kB.
The authors set forth one means by which NF-kB inhibition might favorably effect migraine: a reduction in iNOS. That mechanism may be significant, but the time course is wrong to the extent that a several hour delay between inhibition (or stimulation) and migraine effect is noted.
My experience with migraine suggests that by inhibiting inflammation – through whatever means – the effect on migraine is immediate – within minutes.