中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (7): 1090-1098.doi: 10.4103/1673-5374.187041

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

电针调节ERK1/2信号通路减轻脑缺血再灌注损伤

  

  • 出版日期:2016-07-30 发布日期:2016-07-30
  • 基金资助:
    中国国家自然科学基金项目（81373748, 81171659, 11574156, 81403136）；江苏省“333工程”项目（BRA2014341）；江苏省科技支撑计划项目（BE2010769）

Electroacupuncture alleviates cerebral ischemia and reperfusion injury via modulation of the ERK1/2 signaling pathway

Xiao-lu Jin1, #, Peng-fei Li2, #, Chun-bing Zhang2, 3, Jin-ping Wu3, Xi-lian Feng1, Ying Zhang1, Mei-hong Shen1, *   

  1. 1 Second Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China 2 Department of Clinical Laboratory, Jiangsu Province Hospital of Traditional Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China 3 College of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu Province, China
  • Online:2016-07-30 Published:2016-07-30
  • Contact: Mei-hong Shen, Ph.D., 13815894855@163.com.
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 81373748, 81171659, 11574156 and 81403136; a grant from the 333 Project of Jiangsu Province in China No. BRA2014341; and a grant from the Jiangsu Province Science and Technology Support Project in China, No. BE2010769.

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摘要：

作者既往研究发现电针可以抗氧化应激，保护活性氧损伤所致的疾病，但尚不了解电针对脑缺血再灌注损伤神经保护作用是否通过ERK1/2通路的调控。为此，实验应用大脑中动脉闭塞2 h后再灌注24 h方法建立脑缺血再灌注损伤模型，于再灌注开始时给予大鼠百会和大椎电针刺激30 min，深度10mm，3Hz连续波，强度1-3mA。发现电针刺激能显著缩小脑缺血再灌注损伤大鼠的脑梗死体积，降低缺血大脑皮质中BaxmRNA表达，提高Bcl-2mRNA表达，恢复谷胱甘肽等内源性抗氧化系统活性，降低Nrf2和谷氨酰半胱氨酸合成酶表达，减轻神经元损伤，改善神经功能；但当ERK1/2活性被其特异性抑制剂PD98059抑制时，上述神经保护作用明显减弱。由此说明ERK1/2信号通路的激活既可能参与电针对脑缺血再灌注的神经保护过程。 

orcid: 0000-0002-8650-2778 (Mei-hong Shen)

关键词: 神经再生, 电针, 脑缺血再灌注损伤, 大脑中动脉闭塞, MAPK, 氧化应激, Nrf2, 谷胱甘肽还原酶, 谷胱甘肽, 谷胱甘肽过氧化物酶, Bcl-2

Abstract: Electroacupuncture (EA) has anti-oxidative and anti-inflammatory actions, but whether the neuroprotective effect of EA against cerebral ischemia-reperfusion (I/R) injury involves modulation of the extracellular regulated kinase 1/2 (ERK1/2) signaling pathway is unclear. Middle cerebral artery occlusion (MCAO) was performed in Sprague-Dawley rats for 2 hours followed by reperfusion for 24 hours. A 30-minute period of EA stimulation was applied to both Baihui (DU20) and Dazhui (DU14) acupoints in each rat (10 mm EA penetration depth, continuous wave with a frequency of 3 Hz, and a current intensity of 1–3 mA) when reperfusion was initiated. EA significantly reduced infarct volume, alleviated neuronal injury, and improved neurological function in rats with MCAO. Furthermore, high mRNA expression of Bax and low mRNA expression of Bcl-2 induced by MCAO was prevented by EA. EA substantially restored total glutathione reductase (GR), glutathione (GSH) and glutathione peroxidase (GSH-Px) levels. Additionally, Nrf2 and glutamylcysteine synthetase (GCS) expression levels were markedly increased by EA. Interestingly, the neuroprotective effects of EA were attenuated when ERK1/2 activity was blocked by PD98059 (a specific MEK inhibitor). Collectively, our findings indicate that activation of the ERK1/2 signaling pathway contributes to the neuroprotective effects of EA. Our study provides a better understanding of the regulatory mechanisms underlying the therapeutic effectiveness of EA.

Key words: "nerve regeneration, electroacupuncture, ischemia and reperfusion injury, middle cerebral artery occlusion, mitogen-activated protein kinase, oxidative stress, nuclear factor erythroid 2-related factor 2, glutamylcysteine synthetase, glutathione reductase, B cell lymphoma 2, glutathione peroxidase"