首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Neurochemical Mechanism of Electroacupuncture: Anti-Injury Effect on Cerebral Function after Focal Cerebral Ischemia in Rats
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Neurochemical Mechanism of Electroacupuncture: Anti-Injury Effect on Cerebral Function after Focal Cerebral Ischemia in Rats

机译:电针的神经化学机制:对大鼠局灶性脑缺血后脑功能的抗损伤作用

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We explored the neurochemical mechanism of electroacupuncture's (EA) protective effect on brain function in focal cerebral ischemia rats, using cerebral ischemia/reperfusion rats established by the middle cerebral artery occlusion (MCAO) method. Adult male Sprague–Dawley rats were randomly divided into four groups: Sham, Sham+EA, MCAO and MCAO+EA. The rats in Sham+EA and MCAO+EA were accepted EA treatment at ‘GV26’ and ‘GV20’ acupoints for 30 min. Electric stimulation was produced by a G-6805 generator and neurological deficit scores were recorded. Mitochondria respiratory function and the activities of respiratory enzymes were measured by a computer-aided Clark oxygen electrode system. Results showed that EA treatment might reduce the neurological deficit score, and significantly improve respiratory control ratio (RCR), the index of mitochondrial respiratory function, and increase the activities of succinic dehydrogenase, NADH dehydrogenase and cytochrome C oxidase in the MCAO rats. Results suggest that EA might markedly decrease the neurological deficit score, promote the activities of respiratory enzymes and reduce the generation of reactive oxygen species (ROS), resulting in improvement of respiratory chain function and anti-oxidative capability of brain tissues in the infarct penumbra zone. This be a mechanism of EA's anti-injury effect on brain function in MCAO rats.
机译:我们使用脑中动脉闭塞(MCAO)方法建立的脑缺血/再灌注大鼠,探索了电针(EA)对局灶性脑缺血大鼠脑功能的保护作用的神经化学机制。成年雄性Sprague–Dawley大鼠随机分为四组:Sham,Sham + EA,MCAO和MCAO + EA。 Sham + EA和MCAO + EA的大鼠分别在“ GV26”和“ GV20”穴位接受EA治疗30分钟。由G-6805产生器产生电刺激,并记录神经功能缺损评分。通过计算机辅助的Clark氧电极系统测量线粒体的呼吸功能和呼吸酶的活性。结果表明,电针治疗可能降低MCAO大鼠的神经功能缺损评分,并显着改善呼吸控制率(RCR),线粒体呼吸功能指数,并增加琥珀酸脱氢酶,NADH脱氢酶和细胞色素C氧化酶的活性。结果表明,EA可能会显着降低神经功能缺损评分,促进呼吸酶的活性并减少活性氧(ROS)的产生,从而改善梗死区半影区呼吸链功能和脑组织的抗氧化能力。这是EA对MCAO大鼠脑功能的抗损伤作用机制。

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