Electroacupuncture attenuates cervical spinal cord injury following cerebral ischemia/reperfusion in stroke‑prone renovascular hypertensive rats

Tan,Feng; Chen,Jie; Liang,Yangui; Gu,Minhua; Li,Yanping; Wang,Xuewen; Meng,Di

doi:10.3892/etm.2014.1619

Electroacupuncture attenuates cervical spinal cord injury following cerebral ischemia/reperfusion in stroke‑prone renovascular hypertensive rats

Authors:
- Feng Tan
- Jie Chen
- Yangui Liang
- Minhua Gu
- Yanping Li
- Xuewen Wang
- Di Meng
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Affiliations: Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Foshan, Guangdong 528000, P.R. China, Department of Chinese Medicine, Dongsheng Hospital, Guangzhou, Guangdong 510120, P.R. China
Published online on: March 12, 2014 https://doi.org/10.3892/etm.2014.1619
Pages: 1529-1534

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Abstract

Cerebral ischemia induces injury, not only in the ischemic core and surrounding penumbra tissues, but also in remote areas such as the cervical spinal cord. The aim of the present study was to determine the effects of electroacupuncture (EA) on cervical spinal cord injury following cerebral ischemia/reperfusion in stroke‑prone renovascular hypertensive (RHRSP) rats. The results demonstrated that neuronal loss, which was assayed by Nissl staining in the cervical spinal cords of RHRSP rats subjected to transient middle cerebral artery occlusion (MCAO), was markedly decreased by EA stimulation at the GV20 (Baihui) and GV14 (Dazhui) acupoints compared with that in rats undergoing sham stimulation. Quantitative polymerase chain reaction and western blot analysis demonstrated that EA stimulation blocked the MCAO‑induced elevated protein expression levels of glial fibrillary acidic protein and amyloid precursor protein in the cervical spinal cord at days 24 and 48. To further investigate the mechanism underlying the neuroprotective role of EA stimulation, the protein expression levels of Nogo‑A and Nogo‑66 receptor‑1 (NgR1), two key regulatory molecules for neurite growth, were recorded in each group. The results revealed that EA stimulation reduced the MCAO‑induced elevation of Nogo‑A and NgR1 protein levels at day 14 and 28 in RHRSP rats. Therefore, the results demonstrated that EA reduced cervical spinal cord injury following cerebral ischemia in RHRSP rats, indicating that EA has the potential to be developed as a therapeutic treatment agent for cervical spinal cord injury following stroke.

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