Parthenolide, the presumptive active ingredient in feverfew, might be beneficial in migraine and multiple sclerosis due to inactivation of inducible nitric oxide synthase.
Parthenolide, though previously shown to inhibit NF-kB, was shown in the study summarized below to inhibit NO production through an alternate pathway. It is likely that parthenolide (the presumptive active component of feverfew) acts by various mechanisms in the body.
The investigators conclude that parthenolide might be useful in the treatment of those conditions where excess NO is believed to play a significant role, specifically multiple sclerosis and migraine.
However, it is increasingly recognized that NO plays a key role in disease onset and progression in many conditions related to inflammation, including especially cancer, asthma, inflammatory bowel disease, many autoimmune conditions, and pain itself.
Inhibition of MAP kinase activation and NO synthesis by parthenolide in primary microglial cells.
Summary of the abstract
Nitric oxide (NO) has been implicated in the cause of several conditions affecting the central nervous system, including multiple sclerosis.
Inhibition of NO synthesis has been proposed to be a possible mechanism of action of relevance in the treatment of multiple sclerosis and migraine.
The effect of parthenolide on inducible NO synthase and NO release was investigated in rats, by analysis of their microglia.
Parthenolide (the presumed active ingredient in feverfew) was found to be an inhibitor of NO synthesis. Parthenolide inhibits the activation of mitogen-activated protein kinase (MAPK), but not NF-kB activation.
The data suggest that parthenolide might have a potential in the treatment of central nervous system conditions like multiple sclerosis and migraine, where NO is part of the pathophysiology.