Ren Li, Wang Yu-Kai, Fang Yan-Nan, Zhang Ai-Wu, Li Xian-Liang
Department of Neurology, Affiliated Hospital of Foshan City, Chancheng District Central Hospital of Guangdong Medical College, China.
Neurol Res. 2010 Dec;32(10):1110-6. doi: 10.1179/016164110X12700393823453. Epub 2010 May 18.
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.
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.
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).
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.
