| Background and Objective: Presently, cerebral infarction has become a main disease that threatens the health of middle-aged and elderly people. With the improvement of treatment and health care, its mortality has been significantly declined. However, the sequelae of neurologic deficits caused by cerebral infarction lead to a heavy burden to patient and society. In order to ameliorate the quality of patient's life, the further study will focus on the investigations of prevention and treatment strategies. Disability as a leading consequence of neurological deficits after stroke is due to that poor neurite outgrowth and neurogenesis or increasing neurogenesis but not non-function cannot rebuild normal nervous structure following injury of central nervous system. Recent studies have demonstrated that neurite outgrowth and neurogenesis involve the inhibiting factors derived from myelin such as Nogo-A, myelin associated glycoprotein(MAG), oligodendrocyte-myelin glycoprotein(OMgp), in particular, Nogo-66 receptor plays an important role in the regulation of process.It has been reported that electric stimulation can not only promote recovery of limb motor function and improvement of learning and memory, but also reduce cerebral infarct volume and increase expression of protective protein factors in brain after cerebral infarction. More studies of electric stimulation for hemiparalysis limb have been seen after cerebral infarction, whereas few experiments concentrate on bilateral limb with treatment of electric stimulation. Clinic studies have also found in patients with cerebral infarction that the amelioration of neurologic function by bilateral electric stimulation is better than that by the therapy of hemiparalysis limb; however , the mechanism of treatment with electric stimulation has not been fully clarified. In the present study, we focus on the influence of hemiparalysis limb and bilateral electric stimulation on recovery of neurologic deficit and expression of Nogo-A and Nogo-66 receptor in experimental cerebral infarction rats, which provide evidence in treatment and rehabilitation of cerebral infarction with electric stimulation.Methods: Adult male Sprague-Dawley (SD) rats were randomly divided into normal (8 rats), sham operation, control, impaired limb and bilateral electric stimulation groups (each group including 32 rats). Acute cerebral infarction model was mimicked using middle cerebral artery occlusion (MCAO) techniques. After cerebral infarction for 24h, the rats were treated with or without electric stimulation everyday according to different groups. All groups were treated for 6d with 1d rest, excluding 3d group. 8 rats were selected from every group for evaluating motor function and the expression of Nogo-A and NgR in the border zone of cerebral infarction using beam walking test (BWT) and immunohistochemistory.Results: The motor function was significantly improved in treated groups with electric stimulation compared with control group (P<0. 05). In addition, the effect of bilateral electric stimulation on recovery of motor function was better than that of impaired limb treatment. Further studies have demonstrated that the expression of Nogo-A and NgR was remarkably increased in control and treatment groups after cerebral infarction for 3d (F<0.05) in contrast to sham group, and decreased after 7d and returned to basal level following 21d, whereas no significant change was observed in normal and sham operation groups at each time points. When compared with control group, the expression of Nogo-A and NgR in treatment groups was significantly reduced after cerebral infarction for 3d; however, no significant difference was seen following 21d. In contrast to the impaired limb electric stimulation group, the expression of Nogo-A and NgR in the bilateral treatment group was lower after 7d cerebral infarction (P<0.05), and backed to the same level of impaired limb treatment group after 14d.Conclusions:1. Treatment of acute cerebral infarction with electric stimulation, in particular bilateral stimulation, can improve the movement of the paralyzed extremities.2. Electric stimulation, especially bilateral stimulation can downregulate the expression of Nogo-A and NgR. The improvement of motor function by electric stimulation involves the inhibition of Nogo-A and NgR expression after acute cerebral infarction. |
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