Objective To observe the effect of electroacupuncture(EA) at "Baihui"(GV20)

"Shuigou"(GV26)

etc. on the expressions of vascular endothelial growth factor(VEGF)

collagen fibrillary acidic protein(GFAP)

neuronal nucleus antigen(NeuN)

β-catenin and Axin2 protein and mRNA in rats with cerebral ischemia(CI)

so as to explore its mechanism underlying improvement of ischemic stroke. Methods A total of 108 male SD rats were randomly divided into control

model and EA groups

which were further divided into 7 d

14 d and 21 d subgroups

with 12 rats in each group. The CI model was established by occlusion of the middle cerebral artery. EA(2 Hz/100 Hz

2—4 V) was applied to GV20

GV26

bilateral "Sanyinjiao"(SP6) and bilateral "Neiguan"(PC6) for 30 min

once daily(except Sundays) for 21 days at most. The neurological deficit score was evaluated according to Longa's methods. The cerebral infarction state was assessed by using a magnetic resonance T2 imaging system. The expression levels of neurovascular markers as VEGF

GFAP and NeuN

and β-catenin and Axin2 protein and mRNA in the ischemic brain tissue were detected by using immunohistochemistry and quantitative real-time PCR

respectively. Results After modeling

the neurological deficit score and cerebral infarction size were significantly increased(P<0.01)

and the expression of NeuN and Axin2 proteins and mRNAs were significantly and gradually decreased with time(day 7

14 and 21)(P<0.01)

whereas the expression levels of VEGF

GFAP

β-catenin proteins and mRNAs were significantly increased on day 7

14 and 21 in the model group relevant to the control group(P<0.01). Compared with the model group

the neurological deficit score

cerebral infarction size and the expressions of Axin2 protein and mRNA were significantly decreased on day 7

14 and 21(P<0.01)

whereas the expression levels of VEGF

GFAP and NeuN and β-catenin proteins and mRNAs were considerably up-regulated in the EA group on day 7

14 and 21(P<0.01). Conclusion EA can protect the neurovascular units from injury

reduce the volume of cerebral infarction and improve the symptoms of neurological deficit in cerebral ischemic rats

which may be related to its effects in up-regulating β-catenin expression and in down-regulating Axin2 expression to further activate classical Wnt/β-catenin signal pathway.