Objective  

    To observe the expression of netrin-1 (Ntn1) and semaphorin-3a (sema3a) in the cortex of rats after middle cerebral occlusion (MCAO)

and determine the effect of electro-acupuncture (EA) intervention on their expression

so as to explore the roles of Ntn1 and sema3a in neural plasticity after cerebral infarction.       Methods      A total of 130 male Sprague Dawley (SD) rats were randomly divided into control group (n=10)

model group (n=60) and EA group (n=60

in the acupuncture points PC6 and ST36

80 to 100 Hz

1 to 3 mA

1 to 3 V

for 30 min

performed in 90 min after anesthesia recovery)

and further assigned into 4 time point

that is

in 1

3

7 and 14 d after model establishment. Modified neurologic severity scores (mNSS) were carried out to evaluate neurologic injury at every time point. Immunohistochemical assay was used to detect the expression and distribution of Ntn1

sema3a and NF200 in the cortical ischemic region. Western blotting was employed to detect the expression of Ntn1 and sema3a in the affected cortex.       Results      Immunohistochemical results showed that the rat brain cortex expressed Ntn1 and sema3a at every time point

and they mainly located in the cytoplasm. Western blotting indicated that the model group had higher expression of Ntn1 at 1 d (

P

0.01)

kept in elevation at 3 d (

P

0.01)

reached peak at 7 d (

P

0.01)

and maintained still higherat at 14 d than normal levels (

P

0.01). Compared with the control group

the expression of Ntn1 in EA group had the same trend

but the expression level was significantly higher than the model group

with significant differences in 1

3

7 and 14 d (

P

0.05

P

0.01). Compared with the control group

sema3a protein level in the model group began to rise in 1 d after model surgery (

P

0.01)

increased and reached the peak in 7 d (

P

0.01)

and was still higher than the normal level in 14 d (

P

0.01). Compared to the model group

EA group presented low expression of sema3a at the same time p

oint

with significant differences in 1

3

7 and 14 d (

P

0.05

P

0.01)

and reached peak in 7 d. The results of Western blotting and immunohistochemical assays were basically consistent. Compared with model group

the mNSS of EA group had significant differences in 7 and 14 d (

P

0.05). Significant difference was seen in the expression of NF200 between model group and EA group in 14 d (

P

0.05).       Conclusion      Cerebral infarction significantly up-regulates the expression of Ntn1 and sema3a. EA intervention improves Ntn1 expression but suppresses sema3a

and promotes axon regeneration and repair

which may be one of the mechanisms that EA promotes the recovery of neurological function after cerebral infarction.