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电针通过激活ST36针点中的MD2/TLR4/NF-κB通路来缓解疼痛

Jiangjiang Fu^1,2, Gangchen Cheng^1,2, Zhongxi Lyu^1,2,3

¹School of Acupuncture & Moxibustion and Tuina, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Frontiers in immunology

|February 16, 2026

概括

治疗关节炎疼痛的电针 (EA) 治疗涉及到针点的MD2 / TLR4 / NF-κB通路. 在针点调节MD2为疼痛管理提供了一个潜在的策略,并支持"针点启动"理论.

科学领域:

免疫学和神经科学
分子生物学分子生物学
疼痛管理疼痛管理

背景情况:

针的治疗效果始于针点,NF-κB通路调解了电针 (EA) 的疗效.
了解针点的分子机制对于优化EA治疗至关重要.

研究的目的:

研究MD2/TLR4/NF-κB信号轴在EA介导的止痛中所起的作用.
探索MD2作为疼痛管理的潜在治疗点.

主要方法:

建立了一个辅助剂诱导的关节炎 (AIA) 鼠标模型.
应用EA到Zusanli (ST36) 的针点.
利用行为,分子 (Co-IP,IF) 和遗传 (lentivirus) 方法来分析MD2在针点和脊髓中的功能.

主要成果:

在AIA小鼠中,EA治疗增加了镇痛效应 (脚部热撤回值).
在ST36针点,EA上调调了MD2,TLR4和NF-κB通路组件 (p65,p-p65).
MD2 knockdown部分扭转了EA的止痛作用,而MD2过度表达显示了部分止痛,证实了MD2在MD2/TLR4/NF-κB级联和下游脊髓信号传输中的关键作用.

结论:

这项研究为"针点启动"理论提供了分子证据.
在EA介导的止痛中,MD2通过调节点的MD2/TLR4/NF-κB通路,起到至关重要的作用.
MD2代表了一个有希望的治疗目标,用于开发新的疼痛管理策略.

关键词:

在Grem1/BMP4/COX2路径中.通过MD2/TLR4/NF-κB通路进行.ST36 针点的时间止痛药止痛药止痛药止痛药止痛药电针是一种电针.

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