摘要
目的研究运动训练对脑梗死大鼠神经功能恢复及皮质梗死边缘区突触超微结构与突触素（SYN）含量变化的影响。方法采用Zea—Longa线栓法制作成年sD大鼠左侧大脑中动脉闭塞模型（MCAO）模型，术后按随机数字方法将成模大鼠随机分成运动训练组（r／,=30）和对照组（r／,=30），假手术组（rt=10）。运动训练组从术后48h开始每天予以电动跑笼训练；对照组与假手术组则置于普通笼内饲养，除可自由进食与自主活动外，不予以任何针对性训练。三组大鼠在造模术后第3、7、14、21及35天分别进行神经运动功能评分，随后灌注固定取材，采用透射电镜观察脑皮质梗死边缘区突触超微结构的变化，同时以免疫组化方法（IHC）及蛋白免疫印迹方法（WB）观察脑组织梗死边缘区SYN蛋白的表达。结果在造模术后第7、14、21、35天，运动训练组大鼠的神经运动功能评分[7d：（7．8±0．8）分；14d：（5．6±O．8）分；21d：（3．3±0．8）分；35d：（3．04-0．8）分]均优于对照组[7d：（8．84±0．7）；14d：（7．7±0．9）；21d：（6．9±O．8）；35d：（4．2±0．8），P〈0．05]，且于透射电镜观察下可见运动训练组大鼠皮质梗死边缘区的突触前、后膜结构较完整，突触前膜内囊泡数量增多；而对照组大鼠皮质梗死边缘区的突触结构肿胀明显，突触前、后膜结构模糊，突触前膜内囊泡数量减少。与此同时，运动训练组脑组织梗死边缘区SYN蛋白的表达则在造模术后第21天（0．8±0．1）与第35天（0．7±0．1）均多于对照组（0．44±0．1；0．5±0．1，P〈0．05）。然而在造模术后第3天，不论是神经运动功能评分还是SYN蛋白的表达两组间差异均无统计学意义（均P〉0．05）。结论运动训练能促进脑梗死大鼠运动功能的恢复，其机制可能与脑梗死边缘区突触结构变化及突触素蛋白的表达�
Objective To examine the roles of exercise training in the improvement of damaged neural function and synaptic plasticity. Methods An infarction model was induced by left middle cerebral artery occlusion （MCAO）. A total of 70 adult Sprague-Dawley rats were randomly divided into 3 groups ： physical exercise group （ n = 30） undergoing running wheel exercise daily after MCAO, control group （ n = 30） and sham-operated group （n = 10）. The latter two groups were fed in standard cages without any special training exercise. The rats were scarified at Days 3, 7, 14, 21 and 35 for the evaluation of neural function by neurological severity scores （NSS）. And the synaptic ultrastructures at peri-infarction region were examined by specific marker synaptophysin （SYN）. Results Synaptic ultrastructures at peri-infarction region were observed in both the control and exercise training groups. The presynaptic and postsynaptic membranes were relatively intact. And the presynaptic membranes had more synaptic vesicles from Day 7 post-ischemia. The number of SYN positive cells significantly increased in the exercise training group（21 d： 0. 8±0. 1 ; 35 d：0. 7 ±0. 1）versus those in the control group （21 d：0.4 ±0. 1 ; 35 d：0. 5 ±0. 1） at Days 21 and 35 post-ischemia （P 〈 0.05 ）. Moreover, the neurological severity scores in the exercise traininggroup（7 d：7. 8 ± 0. 8; 14 d：5.6 ± 0. 8; 21 d：3. 3 ± 0. 8; 35 d：3.0 ± 0. 8） showed a quicker declination versus those in the control group （7 d：8. 8 ±0. 7; 14 d：7.7 ±0. 9; 21 d：6. 9 ±0. 8; 35 d：4. 2 ±0. 8）from Day 7 post-isehemia （ P 〈 0. 05）. Conclusion Exercise training plays an important role in the recovery of damaged neural function and synaptic plasticity after cerebral infarction in rats.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2012年第9期628-633,共6页
National Medical Journal of China
基金
国家自然科学基金（81071607、30900547）
广东省科技计划项目（20098030801149）
