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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electroacupuncture Attenuates Cerebral Ischemia and Reperfusion Injury in Middle Cerebral Artery Occlusion of Rat via Modulation of Apoptosis, Inflammation, Oxidative Stress, and Excitotoxicity
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Electroacupuncture Attenuates Cerebral Ischemia and Reperfusion Injury in Middle Cerebral Artery Occlusion of Rat via Modulation of Apoptosis, Inflammation, Oxidative Stress, and Excitotoxicity

机译:通过调节细胞凋亡,炎症,氧化应激和兴奋毒性,电针衰减大鼠中脑动脉闭塞的脑缺血和再灌注损伤

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摘要

Electroacupuncture (EA) has several properties such as antioxidant, antiapoptosis, and anti-inflammatory properties. The current study was to investigate the effects of EA on the prevention and treatment of cerebral ischemia-reperfusion (I/R) injury and to elucidate possible molecular mechanisms. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 24 h. EA stimulation was applied to both Baihui and Dazhui acupoints for 30 min in each rat per day for 5 successive days before MCAO (pretreatment) or when the reperfusion was initiated (treatment). Neurologic deficit scores, infarction volumes, brain water content, and neuronal apoptosis were evaluated. The expressions of related inflammatory cytokines, apoptotic molecules, antioxidant systems, and excitotoxic receptors in the brain were also investigated. Results showed that both EA pretreatment and treatment significantly reduced infarct volumes, decreased brain water content, and alleviated neuronal injury in MCAO rats. Notably, EA exerts neuroprotection against I/R injury through improving neurological function, attenuating the inflammation cytokines, upregulating antioxidant systems, and reducing the excitotoxicity. This study provides a better understanding of the molecular mechanism underlying the traditional use of EA.
机译:电针(EA)具有抗氧化剂,抗炎和抗炎特性的几种性质。目前的研究是探讨EA对脑缺血再灌注(I / R)损伤的预防和治疗的影响,并阐明可能的分子机制。 Sprague-Dawley大鼠对中脑动脉闭塞(MCAO)进行2小时,然后再灌注24小时。在MCAO(预处理)或开始再灌注(处理)之前,每天每天50大,每天刺激刺激30分钟。评估神经系统缺陷分数,梗死体积,脑含水量和神经元细胞凋亡。还研究了相关炎症细胞因子,凋亡分子,抗氧化系统和大脑中兴奋毒性受体的表达。结果表明,EA预处理和治疗均显着降低梗塞体积,脑含水量下降,均匀的大鼠脑含水量下降,减轻神经元损伤。值得注意的是,EA通过改善神经功能功能,衰减炎症细胞因子,上调抗氧化系统并降低兴奋毒性来施加对I / R损伤的神经保护作用。本研究提供了对传统使用EA的分子机制更好地了解。

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