Electroacupuncture alleviates cerebral ischemia and reperfusion injury via modulation of the ERK1/2 signaling pathway.
Electroacupuncture alleviates cerebral ischemia and reperfusion injury via modulation of the ERK1/2 signaling pathway.
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电针通过调节ERK1/2信号通路减轻脑缺血再灌注损伤
DOI：
10.4103/1673-5374.187041
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发表时间：
2016-07
影响因子：
6.1
通讯作者：
Shen MH
中科院分区：
文献类型：
--
作者：
Jin XL;Li PF;Zhang CB;Wu JP;Feng XL;Zhang Y;Shen MH
电针（EA）具有抗氧化和抗炎作用，但电针对脑缺血再灌注（I/R）损伤的神经保护作用是否涉及细胞外调节激酶1/2 （ERK1/2）信号通路的调节尚不清楚。Sprague-Dawley大鼠大脑中动脉闭塞（MCAO） 2小时，再灌注24小时。再灌注开始时，对每只大鼠百会穴（DU20）和大椎穴（DU14）分别施加30分钟的EA刺激（EA穿透深度10 mm，连续波频率3 Hz，电流强度1-3 mA）。EA可显著减少MCAO大鼠的梗死面积，减轻神经元损伤，改善神经功能。此外，EA可抑制MCAO诱导的Bax mRNA高表达和Bcl-2 mRNA低表达，EA可显著恢复总谷胱甘肽还原酶（GR）、谷胱甘肽（GSH）和谷胱甘肽过氧化物酶（GSH- px）水平。此外，EA显著提高了Nrf2和谷氨酰半胱氨酸合成酶（GCS）的表达水平。有趣的是，当ERK1/2活性被PD98059（一种特异性MEK抑制剂）阻断时，EA的神经保护作用减弱。总的来说，我们的研究结果表明，ERK1/2信号通路的激活有助于EA的神经保护作用。我们的研究为EA治疗效果的调节机制提供了更好的理解。
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.