神经炎症
神经保护
实验性自身免疫性脑脊髓炎
小胶质细胞
医学
多发性硬化
兴奋剂
药理学
炎症
电针
调解人
神经科学
神经退行性变
脑脊髓炎
信号转导
病态行为
下调和上调
MAPK/ERK通路
受体
血脑屏障
免疫学
星形胶质细胞
敌手
作者
Yanping Wang,Xiaoru Ma,Zhixin Qiao,Xiyu Zhang,Jiayu Ji,Sifan Zhang,Wei Zhuang,Junfeng Wu,Anqi Li,Chao Wang,Xin Xiu,Jing Wang,Yanting Meng,Wei Huang,Xiujuan Lang,Xijun Liu,B Sun,H L Li,Yumei Liu
标识
DOI:10.1186/s12974-025-03667-1
摘要
Astrocytes are key regulators of neuroinflammation in multiple sclerosis (MS). Electroacupuncture (EA), a safe and cost-effective adjuvant therapy, has shown benefits in neurodegenerative diseases, but its astrocyte-related mechanisms remain unclear. Here, we demonstrated that EA at ST36 alleviated blood-brain barrier (BBB) disruption and neuroinflammation during the peak period of experimental autoimmune encephalomyelitis (EAE). Additionally, EA at ST36 upregulated the expression of α-melanocyte-stimulating hormone (α-MSH) and its receptor melanocortin-4 receptor (MC4R) in spinal astrocytes. Pharmacological studies showed that MC4R agonist RO27-3225 mimicked the therapeutic effects of EA, whereas MC4R antagonist TCMCB07 weakened EA-mediated BBB protection and neuroinflammation suppression. Moreover, astrocyte-specific silencing of MC4R via adeno-associated virus (AAV) weakened EA-mediated BBB protection and neuroinflammation suppression. RNA-sequencing (RNA-seq) and western blot (WB) revealed that EA exerts neuroprotective effects by activating MC4R to inhibit MAPK and NF-κB signaling pathways. Moreover, in MC4R-overexpressing astrocytes, α-MSH and RO27-3225 reduced inflammation responses, while TCMCB07 reversed the effects by MAPK/NF-κB signaling pathways. Collectively, our findings identify astrocytic MC4R as a critical mediator of EA-driven neuroprotection by suppressing MAPK/NF-κB signaling, providing mechanistic insight and a promising therapeutic target for EAE and other neuroinflammatory disorders.
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