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Objective: To observe the expression of Na(v)1.1 and Na(v)1.6 after the electroacupuncture therapy (ET) on acute cerebral ischemia, and discuss the mechanism of function of ET., Methods: Focal acute cerebral ischemia model was established by the occlusion of right middle cerebral artery. Rats were randomly divided into sham operation control (SC), ischemia control (IC) and ET groups. Four acupoints, 'NEIGUAN', 'WAIGUAN', 'SANYINJIAO', and 'ZUSANLI', were selected to be acupunctured. Immunofluorescence and real-time PCR methods were used to detect Na(v)1.1 and Na(v)1.6 expression, and 2,3,5-triphenyl tetra-zolium chloride staining was used to detect infarct volume at 6 hours, 1, 2, 3, and 7 days after ischemia., Results: There is no change in the expression of Na(v)1.1 and Na(v)1.6 in SC group. After ischemia the expression of Na(v)1.1 and Na(v)1.6 was up-regulated compared with that of SC group. The Na(v)1.1 expression was down-regulated from 6 hours to 2 days, then up-regulated from 3 to 7 days. The Na(v)1.6 expression was up-regulated from 6 hours to 1 day, then down-regulated from 2 to 7 days after ischemia. In ET group the neurological deficit behavior, the change in Na(v)1.1 and Na(v)1.6 expression, and the infarct volume were more dramatic than those in IC group at the same time point, and the difference had a statistic value (P<0.05)., Conclusion: Na(v)1.1 and Na(v)1.6 play a role in the injury of cerebral ischemia, ET could regulate the expression of Na(v)1.1 and Na(v)1.6 after ischemia, reduce the infarction volume and decrease cerebral ischemic damage. ET had a cerebral protective function, and one of its important mechanism may be it could regulate the expression of Na(v)1.1 and Na(v)1.6 after ischemia.

Objective: To observe the expression of Nav1.1 and the effect of electroacupuncture therapy (ET) on it after acute cerebral ischemia., Methods: Focal acute cerebral ischemic model was established by occluding right middle cerebral artery. One hundred and forty-five male adult Sprague-Dawley rats were randomly divided into four groups: sham operation group, middle cerebral artery occlusion (MCAO) group, ET group and riluzole group. Double immunofluorescence and real-time PCR were used to observe Nav1.1 expression, and TTC staining was used to detect infarct volume at 6 hours, 1 day, 2 days, 3 days and 7 days after ischemia., Results: The expression of Nav1.1 in sham operation group had no change. After ischemia, the expression of Nav1.1 was up-regulated evidently at 6 hours compared with sham operation group, down-regulated at 1 day and up-regulated again from 2 to 7 days after ischemia; the expression at 7 days was lower than that at 6 hours. In ET group and riluzole group, Nav1.1 expression were down-regulated compared with that in MCAO group after ischemia, the infarct volume was smaller than that in MCAO group at the same time point, and the difference is significant (p<0.05); however, the difference between ET group and riluzole group is not significant (p>0.05)., Conclusion: ET and riluzole could regulate the expression of Nav1.1 after ischemia, decrease the infarction volume and reduce cerebral ischemic injury. One of the important mechanisms for ET's cerebral protective function may be that it could regulate the expression of Nav1.1 after ischemia.