Objective To observe the effect of electroacupuncture(EA)on the expression of myelin basic protein(MBP)

axon growth inhibitor Nogo-A and Nogo receptor(NgR) in corpus callosum of rats with focal cerebral ischemia

so as to explore the mechanism of EA underlying improving ischemic white matter injury. Methods Fourty male SD rats were randomly divided into normal

sham operation

model and EA groups

with 10 rats in each group. The focal cerebral ischemia rat model was established by occlusion of the middle cerebral artery(MCAO). EA was applied to “Baihui”(GV20) and “Zusanli”(ST36) on the left side for 30 min

once daily for 14 days. Neurological function score and the adhensive removal test were used to evaluate neurological deficit severity; Hematoxylin-esion staining was used to observe the pathological changes in myelin of corpus callosum and luxol fast blue(LFB) staining was used to observe the myelin of corpus callosum. Immunohistochemical staining and Western blot were used to detect the expressions of MBP、Nogo-A and NgR in the ischemic corpus callosum.Results After MCAO

the neurological function score was significantly increased(P

<

0.05)

the time required for contact with tape and tape removal was longer(P

<

0.001)

the intensity of LFB staining and the expression of MBP decreased

while the veside area and the expression of Nogo-A and its receptor NgR increased(P

<

0.01

P

<

0.05) in the model group relevant to the normal and sham operation groups. The fiber arrangement of the corpus callosum on the ischemic side was disordered and a large amount of myelin sheath was lost in the model group. Following the treatment

the neurological deficit score of EA group was gradually decreased and significantly decreased on the 3

(rd)

7(rd)

7

(th)

and 14(th) and 14

(th)

day(P

<

0.05)

and the time to remove the adhesive tape was shortened at the 7(th) day(P

<

0.05)

and the time to remove the adhesive tape was shortened at the 7

(th)

and 14(th) and 14

(th)

day(P

<

0.001). The shape of the corpus callosum in the EA group was close to normal

and the myelin structure was relatively complete. The intensity of LFB staining and the expression of MBP was increased(P

<

0.05

P

<

0.01) while the expression of Nogo-A and its receptor NgR were decreased in the EA group relevant to the model group(P

<

0.01). Conclusion EA can play a protective role in myelin of the corpus callosum after cerebral ischemia

which may be related to down-regulating the expressions of Nogo-A and NgR.