CNS neuroscience & therapeutics · 2025
CXCL10 Involvement in Vestibular Migraine via the PI3K/AKT Signaling Pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Song Mao-Mei, Chen Ting-Yan, Song Shi-Na, Gao Ying-Jie, Li Chang-Xin, Xu Sui-Yi
Аннотация
AIMS: C-X-C motif chemokine ligand 10 (CXCL10) is a member of the CXC chemokine family, known as a classical pain-related chemokine. While CXCL10 is implicated in neuropathic pain, its role in vestibular migraine (VM) remains unclear.
METHODS: Serum CXCL10 levels correlated with dizziness and headache severity in VM patients. In the rat VM model, CXCL10, C-X-C motif chemokine receptor 3 (CXCR3), and phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway expression were evaluated to explore the potential mechanisms of CXCL10 in VM.
RESULTS: Serum CXCL10 levels in VM patients were significantly elevated and positively correlated with headache and dizziness severity. In the rat VM model, CXCL10 and CXCR3 expression in the trigeminal nucleus caudalis and vestibular nuclei were significantly increased. Additionally, molecules related to the PI3K/AKT signaling pathway and downstream inflammatory factors showed significantly elevated expression.
CONCLUSION: CXCL10 activates the PI3K/AKT signaling pathway, promoting the release of inflammatory factors, including interleukin-1β, interleukin-6, and tumor necrosis factor-α, and is thus involved in the pathogenesis of VM.
METHODS: Serum CXCL10 levels correlated with dizziness and headache severity in VM patients. In the rat VM model, CXCL10, C-X-C motif chemokine receptor 3 (CXCR3), and phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway expression were evaluated to explore the potential mechanisms of CXCL10 in VM.
RESULTS: Serum CXCL10 levels in VM patients were significantly elevated and positively correlated with headache and dizziness severity. In the rat VM model, CXCL10 and CXCR3 expression in the trigeminal nucleus caudalis and vestibular nuclei were significantly increased. Additionally, molecules related to the PI3K/AKT signaling pathway and downstream inflammatory factors showed significantly elevated expression.
CONCLUSION: CXCL10 activates the PI3K/AKT signaling pathway, promoting the release of inflammatory factors, including interleukin-1β, interleukin-6, and tumor necrosis factor-α, and is thus involved in the pathogenesis of VM.