Electro-Acupuncture Therapy Alleviates Post-Stroke Insomnia by Regulating Sirt1 and the Nrf2-ARE Pathway.

IF 3.3 4区 医学 Q2 NEUROSCIENCES
Yiming Wang, Yifei Chen, Jianbo Yang, Wei Sun, Xiaoning Zhang
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引用次数: 0

Abstract

Post-stroke insomnia (PSI) is a common complication following stroke, which seriously affects patients' life quality. Electro-acupuncture (EA) is an innovative form of traditional Chinese acupuncture that combines electricity with needles to achieve the prevention and treatment of diseases. However, there is limited understanding regarding the treatment mechanism of EA in PSI. In our study, we aimed to investigate the role of EA on PSI development. Our study findings indicated that the quality of sleep, levels of neurotransmitters 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (γ-GABA), and antioxidant levels showed significant improvement following EA treatment in PSI clinical samples and rat models, while the levels of pro-inflammatory factor interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), and astrocyte damage were notably reduced. Furthermore, it was discovered that the levels of sirtuin 1 (Sirt1) were reduced in PSI, a condition that was significantly ameliorated by EA treatment. Additionally, the inhibition of Sirt1 caused a marked elevation in astrocyte apoptosis, inflammatory response, and oxidative stress. Besides, the nuclear factor E2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway was deactivated in the PSI rat model and Sirt1-silenced cells. However, the suppressive impact was successfully counteracted by EA or estazolam (ES), and the overexpression of Nrf2 partially alleviated the increase in apoptosis, inflammation, and oxidative stress caused by Sirt1 knockdown. Taken together, these findings indicated that EA improved sleep quality and silenced Sirt1-induced apoptosis, inflammation, and oxidative stress in PSI by activating the Nrf2-ARE pathway.

电针疗法通过调节Sirt1和Nrf2-ARE通路缓解脑卒中后失眠
脑卒中后失眠是脑卒中后常见的并发症,严重影响患者的生活质量。电针(EA)是中国传统针灸的一种创新形式,将电与针结合起来,实现疾病的预防和治疗。然而,对于EA在PSI中的治疗机制了解有限。在我们的研究中,我们旨在探讨EA在PSI发展中的作用。我们的研究结果表明,EA治疗后PSI临床样本和大鼠模型的睡眠质量、神经递质5-羟色胺(5-HT)和γ-氨基丁酸(γ-GABA)水平和抗氧化水平均有显著改善,而促炎因子白介素6 (IL-6)、肿瘤坏死因子α (TNF-α)水平和星形胶质细胞损伤水平均显著降低。此外,研究发现PSI患者sirtuin 1 (Sirt1)水平降低,EA治疗可显著改善这种情况。此外,Sirt1的抑制导致星形细胞凋亡、炎症反应和氧化应激的显著升高。此外,核因子e2相关因子2 (Nrf2)-抗氧化反应元件(ARE)通路在PSI大鼠模型和sirt1沉默细胞中失活。然而,EA或estazolam (ES)成功地抵消了这种抑制作用,Nrf2的过表达部分缓解了Sirt1敲低引起的细胞凋亡、炎症和氧化应激的增加。综上所述,这些发现表明,EA通过激活Nrf2-ARE通路,改善了睡眠质量,抑制了sirt1诱导的PSI细胞凋亡、炎症和氧化应激。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
NeuroMolecular Medicine
NeuroMolecular Medicine 医学-神经科学
CiteScore
7.10
自引率
0.00%
发文量
33
审稿时长
>12 weeks
期刊介绍: NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.
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