Migraine is a disease of inflammation. NF-kappaB acts as a master switch controlling that inflammation.
Emerging consensus recognizes the importance, in migraine, of the over-production of:
- TNF – NF-kappaB controls it.
- iNOS (NO) – NF-kappaB controls it.
- CGRP – NF-kappaB at least affects it, perhaps critically, perhaps entirely.
Therefore, by inhibiting NF-kappaB, a reduction in each of the above mediators of migraine inflammation might be achieved.
Inhibition of NF-kappaB might be achieved most effectively, and certainly most safely, with the use of natural NF-kappaB inhibitors.
The publication:
August, 2006
Naturally occurring NF-kappaB inhibitors.
Summary of the abstract
NF-kappaB is a ubiquitous and well-characterized protein responsible for the regulation of complex phenomena, with a pivotal role in controlling cell signaling in the body under certain physiological and pathological conditions.
Among other functions, NF-kB controls the expression of genes encoding the pro-inflammatory cytokines (e. g., IL-1, IL-2, IL-6, TNF-alpha, etc.), chemokines (e. g., IL-8, MIP-1alpha, MCP1, RANTES, eotaxin, etc.), adhesion molecules (e. g., ICAM, VCAM, E-selectin), inducible enzymes (COX-2 and iNOS), growth factors, some of the acute phase proteins, and immune receptors, all of which play critical roles in controlling most inflammatory processes.
Since NF-kappaB represents an important and very attractive therapeutic target for drugs to treat many inflammatory diseases, including arthritis, asthma, and the auto-immune diseases, most attention has been paid in the last decade to the identification of compounds that selectively interfere with this pathway.
Recently, a great number of plant-derived substances have been evaluated as possible inhibitors of the NF-kappaB pathway.
