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目的研究脑梗死大鼠运动训练后梗死周边区星形胶质细胞、突触和运动功能的变化及相关性。方法将120只大脑中动脉闭塞脑梗死模型大鼠随机分为康复组、抑制组、盐水组和对照组,以横木行走试验评定运动功能,在7,21,42d应用电镜和免疫组织化学方法,观察各组大鼠脑梗死周边区星形胶质细胞、突触、胶质纤维酸性蛋白和突触素等的变化。结果康复组大鼠3周末的运动功能评分为(3.2±0.3)分,6周末为(5.8±0.9)分,对照组3周末为(1.8±0.5)分,6周末为(2.6±0.8)分;抑制组3周末为(1.6±0.9)分,6周末为(2.1±0.7)分。康复组比对照组和抑制组高,P<0.01。在8000倍电镜视野下,康复组3周末脑梗死周边区星形胶质细胞为(5.8±0.3)个,6周末为(8.5±0.8)个;3周末突触数目为(12.3±1.3)个,6周末为(16.3±1.4)个。星形胶质细胞和突触数目呈同步增多,两者均明显多于对照组和抑制组(P<0.01)。免疫组化染色观察显示,康复组脑梗死周边区胶质纤维酸性蛋白和突触素阳性信号密度值也在3,6周末高于对照组和抑制组(P<0.01)。结论脑梗死大鼠运动训练可促使星形胶质细胞增殖,加强突触重建和功能修复,促进运动功能恢复;星形胶质细胞增殖可能在其中发挥关键性作用。
Objective To study the changes of synaptic and motor function and the correlation of astrocytes in peripheral infarction area after cerebral infarction in rats. Methods One hundred and twenty cerebral infarction rats with middle cerebral artery occlusion (MCAO) were randomly divided into rehabilitation group, inhibition group, saline group and control group. The motor function was evaluated by horizontal walking test. Electron microscopy and immunohistochemistry were performed on 7, 21 and 42 days. The changes of astrocytes, synapse, glial fibrillary acidic protein and synaptophysin in peripheral cerebral infarction group were observed. Results The scores of motor function in the rehabilitation group were (3.2 ± 0.3) at 3 weeks, 5.8 ± 0.9 at 6 weeks, 1.8 ± 0.5 at 3 weeks and 2.6 ± 0.8 at 6 weeks (1.6 ± 0.9) at the end of 3 weeks and (2.1 ± 0.7) at the end of 6 weeks. The recovery group was higher than the control group and the inhibition group, P <0.01. Under the microscope of 8000 times electron microscope, the number of astrocytes in the peripheral zone of the rehabilitation group was (5.8 ± 0.3) at the end of the third week of the rehabilitation group, and was (8.5 ± 0.8) at the end of the sixth week. The number of synapses at the end of the third week was (12.3 ± 1.3) (16.3 ± 1.4) at 6 weeks. The number of astrocytes and synapses increased synchronously, both of which were significantly higher than that of the control group and the inhibition group (P <0.01). Immunohistochemical staining showed that the positive signal density of glial fibrillary acidic protein and synaptophysin in the peripheral area of the rehabilitation group was also higher than that of the control group and the inhibition group at the end of 3 and 6 weeks (P <0.01). Conclusion Exercise training in rats with cerebral infarction can promote astrocyte proliferation, enhance synaptic and functional repair, and promote motor function recovery. Astrocyte proliferation may play a key role in this process.