摘要目的 能评分最高、脑梗死体积最大.假手术组大鼠脑组织中Na(v)1.1表达无变化.缺血后Na(v)1.1表达明显上调,缺血后1d表达下调至最低;真穴位电针组下调与缺血对照组差异有统计学意义(P＜0.05).假穴位电针组下调与缺血对照组相比,差异无统计学意义(P＞0.05).真穴位电针组与假穴位电针组的差异有统计学意义(P＜0.05).结论 电针治疗可以调控Na(v)1.1的表达,缩小脑梗死体积,促进神经功能恢复.电针治疗在缺血后的保护作用可能是通过调控Na(v)1.1的表达来实现.

abstractsObjective To observe the effect of electro-acupuncture therapy (ET) on the expression of sodium channel Na(v) 1.1 in rats after acute cerebral ischemia and the mechanism of any protective function of ET.Methods A model of focal acute cerebral ischemia was established by occluding the right middle cerebral artery.One hundred and eighty healthy SD rats were randomly divided into a sham operation control (SC) group, an ischemia control (IC) group, a real ET group and a false ET group, with 45 in each group. Immunohistochemistry and real-time polymerase chain reaction (PGR) methods were used to detect Na(v)1. 1 expression. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was used to detect infarct volume. Neurological examination and grading was carried out at 6 hours and then 1, 2, 3 and 7 days after inducing ischemia. Results The gradings and infarction volume ratios of the rats in the IC group were the most serious, while in the real ET group the severity was much less at each time point. Compared with the SC group, the expression of Na(v) 1.1 was significantly up-regulated in the IC group. The expression of Na(v) 1.1 was increased at the 6th hour, then down-regulated to the lowest level at day 1,then from the 2nd to the 7th day was up-regulated again. The expression of Na(v) 1.1 in the real ET group was significantly lower than in the IC group. Although the expression of Na(v)1.1 in the false ET group was low compared with the IC group, the difference was not significant. The difference between the real ET group and the false ET group was significant, however. Conclusions ET can reduce damage from cerebral ischemia and benefit the recovery of neural function. ET can also could regulate the expression of Na(v)1.1 after acute cerebral ischemia, which may be an important mechanism for neural function recovery.