Effect of electroacupuncture therapy on the expression of Na(v)1.1 and Na(v)1.6 in rat after acute cerebral ischemia.
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).


CONCLUSIONS
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.
Ren
Li
L
Department of Neurology, Affiliated Hospital of Foshan City, Chancheng District Central Hospital of Guangdong Medical College, China.
Wang
Yu-Kai
YK
Fang
Yan-Nan
YN
Zhang
Ai-Wu
AW
Li
Xian-Liang
XL
D000818:Animals; D020520:Brain Infarction / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D002545:Brain Ischemia / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D004195:Disease Models, Animal; D015671:Electroacupuncture / Q000379:methods*; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D008297:Male; D062550:NAV1.1 Voltage-Gated Sodium Channel; D062557:NAV1.6 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015222:Sodium Channels / Q000096:biosynthesis* / Q000235:genetics
D062550:NAV1.1 Voltage-Gated Sodium Channel; D062557:NAV1.6 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; C568250:Scn1a protein, rat; C507811:Scn8a protein, rat; D015222:Sodium Channels