Abstract

Glial cells are now recognized as an active participant in the initiation and maintenance of migraine. NF-κB, a nuclear transcription factor, is the center of inflammatory response. Nitroglycerin (NTG)-induced NF-ĸB activation has been shown to play a critical role in the pathogenesis of migraine. Nitroglycerin (NTG) can activate NF-κB transcription, leading to the translocation of p65 subunit of NF-κB into the nucleus. Tetrandrine (Tet), a traditional Chinese medicine as a calcium channel blocker and an inflammation antagonist, has been applied in the treatment of various neurologic diseases. Evidence has demonstrated tetrandrine as a potent inhibitor of NF-κB activation in cells. The present study aimed to investigate whether NF-κB activation in the satellite cells can lead to the release of inflammatory cytokines involving in the migraine and to explore the relationship between NF-ĸB and Tet in the pathology of migraine. Male Sprague Dawley rats received injection with nitroglycerin to introduce migraine. Immunohistochemistry, Western blot, and RT-PCR were used to determine the NF-ĸB levels and study the changes under basal conditions in response to tetrandrine injection. A significant increase in the nuclear p65, an indicator of NF- ĸB activation, was detected in the trigeminal ganglia of rats following injection with nitroglycerin. However, the nitroglycerin-induced NF-ĸB activation in the trigeminal ganglia was attenuated by pretreatment with Tet in a dose-dependent fashion. NF-ĸB activation in the trigeminal ganglia is implicated in the pathology of migraine, and Tet may be a novel and promising candidate for future treatment or prevention of migraine via inhibiting NF-ĸB activation in the trigeminal ganglia.

Key words: Tetrandrine, migraine, nuclear factor kappa B and satellite cells.