A 2025 rodent study compared protective effects of sulforaphane and a migraine compound on nitroglycerin-induced migraines:

“Activation of trigeminal vascular pathways and the release of calcitonin gene‐related peptide (CGRP) are central to migraine pathogenesis. The amylin‐1 (AMY1) receptor is expressed in key structures implicated in migraine mechanisms.

This study evaluated protective effects of sulforaphane (SFN) against nitroglycerin induced migraine in female mice, comparing its efficacy to the standard migraine medication, topiramate. Migraine was induced using nitroglycerin (10 mg/kg, i.p., administered every other day), and treatments included sulforaphane (5 mg/kg/day, i.p.) or topiramate (30 mg/kg/day, i.p.) for a duration of 9 days.

Sulforaphane demonstrated significant improvements in behavioral symptoms such as photophobia, head grooming, and both mechanical and thermal allodynia. These behavioral changes were accompanied by reductions in serum levels of nitric oxide, CGRP, and pro‐inflammatory cytokines.

Histological analysis revealed that sulforaphane ameliorated nitroglycerin-induced damage in the trigeminal ganglia and trigeminal nucleus caudalis. Additionally, sulforaphane reduced AMY1 receptor expression in the medulla and inhibited its downstream signaling components, including phosphorylated ERK1/2, P38, and c‐Fos. Sulforaphane further enhanced the Nrf2/HO‐1 pathway while suppressing the NF‐κB/NLRP3/caspase‐1 signaling cascade.

These findings indicate that SFN has a potential as a novel therapeutic candidate for migraine management by targeting the downstream signaling pathways of the AMY1 receptor.”

https://onlinelibrary.wiley.com/doi/10.1002/ardp.70107 “The Role of the AMY1 Receptor Signaling Cascade in the Protective Effect of Sulforaphane Against Nitroglycerin-Induced Migraine in Mice” (not freely available)

This study’s Reference 34 was a 2016 study curated in Do broccoli sprouts treat migraines?.