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: 1 h, 1 d, 3 d, 7 d, and 21 d after CI (n = 6 in each subgroup). The CI model was established by occlusion of the middle cerebral artery. EA (1 - 3 mA) was applied to "Baihui" (GV 20) and "Dazhui" (GV 14) for 30 min, once a day for 1 h, 1 d, 3 d, 7 d and 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 3 and 7 were significantly higher in the model group (P<0. 05), while those of O4 on day 1, 3, 7 and 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. 0 1 , 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.

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