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.
Highlights
Cerebral ischemia induces neuronal cell death at the infarct core and secondary neuronal injury in the surrounding hypoperfused penumbra region, in addition to injuring the remote cervical spinal cord with which it is connected [1]
To explore the neuroprotective role of EA in the cervical spinal cord during cerebral ischemia, Nissl immunocytochemistry was performed to determine the neuronal loss in RHRSP rats
MCAO, middle cerebral artery occlusion; EA, electroacupuncture. It was shown for the first time, to the best of our knowledge, that EA stimulation at GV20 (Baihui) and GV14 (Dazhui) significantly attenuates cerebral ischemia‐induced remote cervical spinal cord neuronal loss and changes in glial fibrillary acidic protein (GFAP), amyloid precursor protein (APP), Nogo‐A and Nogo‐66 receptor‐1 (NgR1) expression in hypertensive rats
Summary
Cerebral ischemia induces neuronal cell death at the infarct core and secondary neuronal injury in the surrounding hypoperfused penumbra region, in addition to injuring the remote cervical spinal cord with which it is connected [1]. Neuronal loss is topographically associated with axonal degeneration and is further induced by remote injury [2]. The mechanisms underlying remote injury remain unclear and no treatment is yet available to reduce remote neuronal loss following cerebral ischemia. Nogo‐A is an inhibitor of neurite growth and is regulated by two inhibitory domains: 66‐amino acid region (Nogo‐66) and the N‐terminal region (amino‐Nogo). The NgR1 competitive antagonist, NEP1‐40 (Nogo‐66 residues 1‐40), blocks this inhibitory effect [6]. The role of Nogo‐A and NgR1 in regulating remote alteration of the cervical spinal cord following cerebral ischemia remains unknown
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