Mechanism of SGCs-HMGB1 axis-mediated peripheral sensitization in migraine based on neuroimmune microenvironment of trigeminal ganglion and traditional Chinese medicine intervention
Abstract
Migraine is a common neurovascular disorder, and its chronification and recurrent attacks are closely associated with peripheral sensitization. Trigeminal ganglion(TG) is an important initial site of peripheral sensitization in migraine, in which neurons and satellite glial cells(SGCs) are major contributors. The neuroimmune microenvironment composed of the two plays a key role in pain signal amplification. Upon external stimulation, neurons and SGCs can release alarmin high mobility group protein B1(HMGB1), which binds to specific receptors to activate inflammasomes, thereby further amplifying local inflammatory responses and neuronal excitability. Previous studies have shown that SGCs activation, HMGB1 externalization, and its downstream inflammatory cascades collectively contribute to neuroimmune imbalance within the TG, and may constitute an important amplification loop driving peripheral sensitization in migraine. In TCM, the pathogenesis of migraine is closely related to wind, heat, phlegm, and blood stasis. These pathological changes are, to some extent, consistent with the dysregulation of the TG neuroimmune microenvironment, the sustained release of inflammatory mediators, and the chronification of pain. In addition, existing studies have systematically indicated that active components of TCM may exert anti-inflammatory and analgesic effects by inhibiting SGCs activation, interfering with HMGB1 release, or blocking its receptors and downstream signaling pathways,…
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