电可以抑制神经元铁亡,以缓解慢性神经病痛
Chunchun Xue1, Wenyun Kui1, Aiping Huang1
1Department of Pain, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Journal of cellular and molecular medicine
|March 21, 2024
概括
电针 (EA) 通过抑制脊髓中细胞死亡途径ferroptosis来缓解神经病痛 (NP). 这种治疗保护神经元并激活Nrf2抗氧化途径,为NP管理提供了一种新的治疗机制.
科学领域:
- 神经科学是一个神经科学.
- 疼痛管理 疼痛管理
- 细胞生物学 细胞生物学
背景情况:
- 慢性神经病痛 (NP) 是一种具有不完全理解机制的衰弱性疾病.
- 铁,一种编程细胞死亡的形式,与NP的发展有关.
- 电疗法 (EA) 通过向ferroptosis显示了神经恢复的希望.
研究的目的:
- 研究EA在治疗慢性收缩损伤 (CCI) 诱导的NP中的机制.
- 为了确定EA的止痛作用是否通过调节脊髓中的铁死来调节.
- 探索Nrf2信号通路在EA神经保护作用中的作用.
主要方法:
- 在雄性Sprague-Dawley大鼠中建立CCI诱导的NP模型.
- 在ST36和GV20针点进行EA治疗,持续14天.
- 评估疼痛过敏,神经元损伤,铁亡标志物 (xCT,GPX4,FTH1,SOD,ACSL4,MDA,铁),以及Nrf2通路的激活.
主要成果:
- EA显著减轻了疼痛过敏和减少了脊髓中神经元损伤.
- 通过对保护性蛋白质 (xCT,GPX4,FTH1,SOD) 的上调和对促费罗性因素 (ACSL4,MDA,铁) 的下调,EA逆转了氧化应激诱导的铁.
- EA激活了Nrf2信号通路,其抑制部分阻断了EA对铁亡和疼痛的保护作用.
结论:
- 在ST36和GV20的EA治疗有效地管理神经病痛.
- 通过抑制脊髓铁亡,EA对NP进行神经保护.
- Nrf2信号通路在介导NP中EA的抗ferroptotic和止痛作用方面发挥着部分作用.
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