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电针促进了巨/微质M2两极分化,并通过AMPK抑制炎症性疼痛
Fu-Bei Nan1, Yi-Xiao Gu2, Jun-Lu Wang1
1Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou.
Neuroreport
|March 25, 2024
概括
电针通过激活腺5'-单酸 (AMP) 激活蛋白激酶 (AMPK) 和静音信息调节器1 (SIRT1) 来缓解炎症性疼痛,促进M2巨/微质两极分化.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 疼痛管理 疼痛管理
背景情况:
- 炎症性疼痛是一个全球性的健康挑战.
- 电针 (EA) 显示出缓解疼痛的希望,但其机制尚不清楚.
- 了解EA的分子通路对于有效的疼痛管理至关重要.
研究的目的:
- 为了研究腺5'-单酸盐 (AMP) 激活蛋白激酶 (AMPK) 和静音信息调节器1 (SIRT1) 在电针的抗毒感受作用中的作用.
- 为了确定AMPK调节的SIRT1是否在炎症性疼痛中调节巨/微质偏振.
- 在炎症性疼痛的小鼠模型中阐明电的潜在机制.
主要方法:
- 带有完整的freund's辅助剂 (CFA) 诱导的炎症性疼痛的小鼠被用电针治疗.
- 评估了机械的全体运动和热性过敏症.
- 西部斑点分析用于测量蛋白质水平,包括AMPK,p-AMPK,SIRT1和免疫标记物. 使用的是AMPK敲除和SIRT1抑制.
主要成果:
- 在用CFA治疗的小鼠中,电显著降低了热过敏症和机械.
- 治疗EA增加了AMPK酸化水平.
- 抑制AMPK可以逆转EA的止痛作用和M2偏振;抑制SIRT1可以减弱EA对M2偏振的影响.
结论:
- 氨酸5'-单酸 (AMP) 激活蛋白激酶 (AMPK) 和静音信息调节器1 (SIRT1) 信号传递对于电的止痛效果至关重要.
- 电可以通过AMPK-SIRT1通路促进M2巨/微质的两极分化.
- 这项研究揭示了电治疗治疗炎症性疼痛的新机制.
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