| The paper consists two parts:literature review and experimental study.First Section:literature SummaryThere are two literature reviews. The first article introduces the research progress of electroacupuncture(EA) treating in craniocerebral injury (CCI) in the past few years, discusses mainly from three aspects as the pathological mechanism of CCI, the clinical surveys and experimental surveys of EA treatment on CCI. The second article introduces the research progress of Nogo-A in the resent years at home and abroad, discusses the relationship between Nogo-A and CCI.Second Section:Experimental Research Objective:To observe the effect of EA on the content of Nogo-A mRNA in brain of acute CCI rat, discuss the protective mechanism of EA in CCI.Methods:Rats were divided into three groups randomly:Blank Group, Model Group and EA Group. The CCI rat model was made by using a modified Feeney s method. The brain tissues were taken at 6h,24h,48h,6d after the model making. (1) Comprehensive evaluation of neural function of CCI rats by a simplified neural injury severity score (NSS) evaluation criteria. (2) The injured tissues of Blank Group, EA Group and Model Group were removed to determine the content of Nogo-A mRNA through RT-PCR.Results:After CCI, (1) Compared with the Blank Group, the NSS in Model Group was significant higher at 6h(P<0.01),24h(P<0.01),48h(P<0.01),6d (P<0.01); Compared with the Model Group, the NSS in EA Group was significant lower at 6h(P<0.01),24h(P<0.05), 48h(P<0.05),6d(P<0.05). (2) Compared with the Blank Group, the content of Nogo-A mRNA in brain of Model Group was significant differently (P<0.01), it was decreased at first, then increased at a level, and decreased again at last; Compared with the Model Group, the content of Nogo-A mRNA in brain of EA Group was increased at 6h(P<0.05), and decreased at 24h(P<0.05),48h (P<0.05),6d(P<0.05).Conclusion:EA has a bi-directional benign regulatory effect on the content of Nogo-A mRNA in brain of acute CCI rats. It may protect the Nogo-A existed in normal nerve cells, and decrease the high level content of Nogo-A in pathological status. This may be one of the therapeutic mechanisms of EA on brain. |