Objective To observe the effect of electroacupuncture(EA)on changes of ultrastructure of oligodendrocytes in the marginal zone of the cerebral ischemia(CI)locus in rats with cerebral infarction so as to reveal its mechanism underlying improving ischemic cerebral diseases.Methods Ninety male SD rats were randomized into sham operation

model and electroacupuncture(EA)groups which were further divided into five subgroups:1h

1d

3d

7d

and 21 dafter CI(n=6in each subgroup).The CI model was established by occlusion of the middle cerebral artery.EA(1-3mA)was applied to"Baihui"(GV20)and"Dazhui"(GV 14)for 30 min

once a day for 1h

1d

3d

7dand 21 d

respectively.The ultrastructural changes of oligodendrocytes in the marginal zone of the ischemic cerebral tissue were observed by transmission electron microscope.The immunoactivity levels of A2B5

O4 and 2'

3'-cyclic-nucleotide 3'-phosphodiesterase(CNPase)for labeling the oligodendrocyte precursor cells

immature oligodendrocytes

and mature oligodendrocytes respectively were detected by immunohistochemistry.Results The oligodendrocytes were swelling in structure and increased in number after cerebral ischemia.Compared with the model group

the degree of swelling of oligodendrocytes was obviously decreased and new oligodendrocyte proliferation was found in the EA group.In comparison with the sham group

the immunoactivity levels of cerebral A2B5 and CNPase proteins on day 3and7 were significantly higher in the model group(P<0.05)

while those of O4 on day 1

3

7and 21 were obviously lower in the model group(P<0.01).Following EA intervention

the immunoactivity levels of cerebral A2B5

O4 and CNPase proteins were significantly up-regulated in the EA group in comparison with the model group(P<0.01

P<0.05).Conclusion EA intervention may reduce the structural damage of oligodendrocytes in CI rats

which may be associated with its effects in promoting the expression of cerebral A2B5

O4 and CNPase proteins

suggesting an involvement of glial cells in the protective effect of EA.