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The aims of this study were to investigate the effects and feasibility of electroacupuncture (EA) therapy for the treatment of traumatic brain injury (TBI) and its underlying mechanism,and to discuss its impact on the repair and regeneration of neurological functions and neuronal plasticity.Eighty female Sprague-Dawley rats were randomly divided into Sham,TBI model,early EA treatment A (treatment at 1 hour after injury) and early EA treatment B (treatment at 72 hours after injury) groups.Moderate brain injury was induced in rats by a free-falling instrument.EA treatments were conducted at 1 hour (Group A) and 72 hours (Group B) after the injury,by selecting the Quchi (LI11) and Zusanli (ST6)asthe main acupointsand piercing to 4 mm.The detailed parameters were: (1) alternating frequency of 2 and 30 Hz (dense and disperse) with an interval of 4 seconds,and (2) an intensity of 1-4 mA.This treatment was given daily for 15 minutes for 14 days.Behavior dysfunction was dynamically monitored on days 1 through 14 after injury by walking and balancing tests.According to the results,behavior disorders were observed in rats with TBI,while recovery of motor functions was improved by EA therapy,with a more significant effect in the group treated earlier.Cerebral edema was measured by the dry-wet method.There was no significant effect of EA treatment on cerebral edema during the acute stage.Next,we used hematoxylin and eosin staining to determine the neuronal necrosis rate in injured cortex and hippocampus.We found that the secondary neuronal necrosis rate was lowered by EA treatment in those areas.In addition,results from immunohistochemical staining showed increased staining for basic fibroblast growth factor-positive neurons.Data collected from in situ hybridization demonstrated that after injury,the expression of growth associated protein-43 (GAP-43) mRNA in the parietal cortex adjacent to the outside of the injured area and in the hippocampal CA1 region of the injured hemisphere was upregulated,followed by an abnormal expression of somatostatin mRNA.Positive staining of hippocampal dentate gyrus neurons in the EA treatment group at 1-3 days after injury was significantly different (P < 0.05) than those in the injured group.Similarly,a significant difference (P < 0.05) was also detectable on day 3 after injury between EA treatment and TBI model groups.Under normal circumstances,the expression of GAP-43 mRNA is maintained at a low level,and positive hybridization signal can usually be detected in the cortex and hippocampus.However,injury increased the expression of GAP-43 mRNA in the cortex outside the injured zone and bilaterally in the hippocampi (more apparent in the injured side),with an expression peak (P< 0.01) at 5 days after injury.This high expression,in contrast to the normal level,lasted for a longer time,as it could still be seen at 14 days after injury.EA treatment affected the post-injury expression of GAP-43 mRNA both temporally and spatially.The peak expression (+++) was induced at 3 days after injury,and lasted until day 7.Although the situation reversed by day 14 after injury,expression was still higher than normal level (P < 0.05),illustrating the role of EA treatment in regulating the expression of GAP-43 mRNA and improving the post-injury neuronal regeneration.In summary,our study suggested that although EA treatment had no significant effect on acute cerebral edema,cerebral hematoma,or mortality of the animals,early use of the therapy does help relieve the secondary progression of post-injury pathological processes and supports the regeneration and repair of injured neurons and recovery of brain functions.