Objective To explore the mechanism of electroacupuncture(EA) underlying improvement of cerebral infarction(CI) by investigating its influence on expression of cerebral Wnt7 a

lymphoid enhancer factor-1(LEF1)

glycogen synthase kinase 3β(GSK-3β) and Dickkopf-1(DKK1) mRNA and proteins in CI rats. Methods A total of 280 male Wistar rats were randomly divided into blank control(n=10)

sham-operation

model and EA groups

and 90 rats of the last 3 groups were further divided into 1

3

6

9

12 and 24 h

and 3

7 and 12 d subgroups with 10 rats in each subgroup. The CI model was established by occlusion of the middle cerebral artery(MCAO). The sham-operation group received the same surgical operation but without thread embolus insertion. EA(2 Hz/15 Hz

2 mA) was applied to "Shuigou"(GV26) for 20 min

once a day for 1

3

7 and 12 d

respectively. The neurological deficit was evaluated by using Neurological Severity Scores(NSS). The expression levels of Wnt7 a

LEF1

GSK-3β and DKK1 mRNAs and proteins in the right ischemic brain tissues were detected by Quantative real-time PCR and Western blot

respectively. Results After MCAO

the NSS score was significantly increased in the model and EA groups relevant to the blank control and sham-operation groups(P<0.01) and gradually decreased with the prolongation of ischemia time. After EA

the NSS scores were notably decreased on day 3

7 and 12 in the EA group compared with the model group(P<0.05

P<0.01). After modeling

the expression levels of Wnt7 a and LEF1 mRNAs from 3 h to 12 d

Wnt7 a and LEF1 proteins from 6 h to 12 d were considerably increased(P<0.01

P<0.05)

while those of GSK-3β mRNA at 9

12 and 24 h

GSK-3β protein at 24 h and 3 d

and DKK1 mRNA at 24 h and 3 d and DKK1 protein at 3 d were obviously decreased in the model group relevant to the sham-operation group(P<0.05

P<0.01). After the intervention

the expression levels of Wnt7 a mRNA at 12 h to 3 d

Wnt7α protein from 24 h to 12 d

LEF1 mRNA from 24 h to 12 d

and LEF1 protein from 3 d to 12 d were further apparently up-regulated(P<0.01

P<0.05)

while those of GSK-3β mRNA at 9 h

3

7 and 12 d

and GSK-3β protein at 12 h

7 d and 12 d

and DKK1 mRNA at 12 h

24 h and 3 d

and DKK1 protein at 24 h to 12 d were obviously down-regulated in the EA group relevant to the model group(P<0.01

P<0.05). No significant difference was found between the blank and sham-operation groups in the NSS scores and expression levels of Wnt7 a

LEF1

GSK-3β and DKK1 mRNAs and proteins at all the time points(P>0.05). Conclusion EA of GV26 can significantly improve the neurological deficit symptoms in MCAO rats

which may be associated with its effects in up-regulating the expression of Wnt7 a and LEF1 mRNAs and proteins

and in down-regulating the expression of GSK-3β and DKK1 mRNAs and proteins.