Therefore, these findings confirmed the mechanism that the integrity of the BBB was altered by NTG or CGRP; subsequently, IL-17A derived from periphery induced neuroinflammation and hypersensitization in the TNC, which gain a deep insight to the IL-17A inflammatory signaling in NTG-induced migraine and revealed that anti-inflammation or BBB protection strategy warrant further research to investigate the availability in clinical treatment. Here, OPA1 is linked to migraine disorder.