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Evidence-Based Complementary and Alternative Medicine
Volume 6, Issue 1, Pages 51-56
Original Article

Neurochemical Mechanism of Electroacupuncture: Anti-Injury Effect on Cerebral Function after Focal Cerebral Ischemia in Rats

1Department of Integrative Medicine and Neurobiology, Shanghai Medical College, Fudan University, Shanghai 200032, China
2Jiangsu Key Laboratory of Acupuncture and Moxibustion, Nanjing University of Traditional Chinese Medicine, Jiangsu, China
3Department of Integrative Medicine and Neurobiology, Shanghai Medical College, Fudan University, No.138, Yi Xue Yuan Road, Shanghai 200032, China

Received 11 September 2006; Accepted 11 April 2007

Copyright © 2009 Shubo Zhong et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.